TOLUMBIA  LIBRARIES  OFFSITE 

HFWiHsaiNf;is;-ji,|ANrJA|<1J  ... 


HX641 29098 
RC683  .H25  1917    The  diagnosis  and  tr 

:■{;   !;:<!   :.        . 

RECAP 


•lVliiMl! 

rn 


!(C  (,'»J 


}U* 


COLUMBIA    UN1VERSIT' 

EDWARD    G     JANEWAY 

MEMORIAL    LIBRARY 


Digitized  by  the  Internet  Archive 

in  2010  with  funding  from 

Open  Knowledge  Commons 


http://www.archive.org/details/diagnosistreatmeOOhart 


THE 

DIAGNOSIS  AND    TREATMENT 

OF 

ABNORMALITIES 

OF 

MYOCARDIAL  FUNCTION 

With  special  reference  to  the  use  of 
GRAPHIC    METHODS 


BY 

T.  STUART  HART,  A.M.,  M.D. 

Assistant    Professor   of    Clinical   Medicine  in  the    College   of   Physicians    and 

Surgeons,  Columbia  University.      Visiting  Physician  to  the 

Presbyterian  Hospital  in  the  City  of  New  York. 

Illustrated  with  248  Engravings, 
240  of  which  are  Original 


CD 

m 

Quo**' 


THE  REBMAN  COMPANY 

NEW  YORK 
1917 


Copyright,  1917.  by 
THE  REBMAN  COMPANY 


All  Right*  Reserved 


PRINTKD  IN  AMI  RICA 


TO 

DOCTOR  WALTER  B.  JAMES 

A  PIONEER  IN 

THE  APPLICATION  OF 

METHODS  OF  PRECISION 

TO  THE  SOLUTION  OF 

CLINICAL  PROBLEMS 

THIS  BOOK  IS  INSCRIBED 

AS  A  TOKEN  OF 
ESTEEM  AND  AFFECTION 


FOREWORD 

In  very  recent  years  there  lias  been  added  to  clinical  medicine  a 
new  chapter  on  the  functional  activity  of  the  heart  muscle.  'I  hei  e 
pages  have  been  written  in  a  language  almost  wholly  new  and  in 
characters  hitherto  unfamiliar. 

In  conducting  a  series  of  lectures  and  laboratory  exercises  on 
cardiac  pathology  during  the  past  live  years  in  Columbia  University 
it  has  become  increasingly  clear  to  the  writer,  that  there  was  needed 
a  manual  which  should  present  the  knowledge  more  recently 
acquired  in  this  field  in  a  simple  and  condensed  form  to  meet  the 
requirements  of  the  student  and  practitioner. 

The  attempt  has  been  made  to  approach  the  subject  from  the 
clinical  side  and  to  lay  stress  on  the  features  which  are  of  practical 
importance  to  those  whose  advice  is  sought  on  these  questions  of 
disordered  cardiac  activity.  We  have  endeavored  to  use  as  simple  a 
vocabulary  as  possible  and  yet  to  introduce  the  terms  which  in  a 
brief  period  must  be  the  daily  companions  of  the  physician  who 
would  be  abreast  of  the  times. 

If  it  should  seem  that  we  have  consumed  too  considerable  a 
portion  of  our  space  in  a  presentation  and  discussion  of  graphic 
records  it  is  because  our  new  knowledge  of  myocardial  function  has 
been  to  a  large  extent  obtained  by  these  agencies,  and  we  believe 
that  these  afford  the  easiest  and  simplest  approach  to  a  clear  com- 
prehension of  the  views  at  present  held.  Today's  literature  is 
teeming  with  these  pictures  of  heart  activity  and  a  familiarity  with 
them  will  make  accessible  the  valuable  additions  which  are  daily 
being  made  to  our  knowledge  in  the  fields  of  myocardial  pathology 
and  therapeutics. 

It  is  not  presumed  that  every  practitioner  will  have  the  time  or 
facilities  to  make  graphic  records  of  those  of  his  patients  in  whom 
he  suspects  a  myocardial  defect,  but  it  is  hoped  that  these  pages  mav 
be  of  service  in  inducing  a  closer  study  of  the  signs  which  are 
obtainable  by  the  more  common  methods  and  may  help  in  the  inter- 
pretation of  the  facts  thus  secured. 

The  theories  of  myocardial  function  as  generally  accepted  at  the 
present  time  have  been  briefly  outlined  together  with  a  few  of  the 
more  important  facts  upon  which  these  hypotheses  rest.  Mam- 
points  which  are  still  in  controversy  have  been  touched  upon,  but 
an  effort  has  been  made  to  avoid  an  extended  argument  on  those 
subjects  which  can  only  be  decided  by  further  investigation. 

The  literature  has  become  voluminous  and  the  papers,  clinical  and 
experimental,  bearing  on  this   subject  are   of  very  great  number. 

v 


•l  IREWORD 


No  attempt  has  been  made  to  present  a  complete  bibliography,  but 
references  have  been  given  to  many  of  the  recenl  important  papers 

and  from  those  the  student  who  is  more  deeply  interested  may  secure 
further  leads  to  special  lines  of  investigation  which  may  he  of  use 
to  him. 

Perhaps,  in  no  other  field,  is  clinical  medicine  a  greater  debtor 
to  the  combined  efforts  of  the  physicist,  physiologist  and  the  patholo- 
gist than  the  one  presented  in  these  pages.  It  is  a  brilliant  illustra- 
tion of  the  practical  results  which  may  be  obtained  by  the  coopera- 
tion of  those  working  in  the  different  sciences.  The  discoveries  of 
pure  physiology  made  accessible  by  the  physicist  and  verified  by 
the  pathologist  have  been  pressed  into  the  service  of  humanity  by 
the  master  clinician.  The  practitioner  is  under  deep  obligation  to  the 
many  investigators  who  have  contributed  to  this  result  and  whose 
names  will  be  found  on  every  page  of  this  book.  For  their  ingenuity 
in  devising  methods  and  their  application  to  clinical  medicine  the 
services  of  James  Mackenzie  and  Willem  Einthoven  will  always 
remain  conspicuous. 

The  investigations  of  the  writer  have  been  conducted  in  the 
Laboratory  of  Physical  Pathology  and  the  Wards  of  the  Pres- 
byterian I  Iospital  and  he  is  deeply  in  debt  to  his  colleagues  in  the 
hospital  for  placing  interesting  cases  at  his  disposal  for  observation 
and  study,  and  to  others  in  several  of  the  departments  of  Columbia 
University  for  counsel  and  assistance. 

He  is  particularly  under  obligation  to  Dr.  Walter  B.  James, 
Clinical  Professor  of  Medicine,  the  founder  of  the  laboratory 
devoted  to  the  study  of  the  heart  by  physical  methods  in  the  Pres- 
byterian Hospital;  to  Dr.  Warfield  T.  Longcope,  Professor  of  Medi- 
cine and  Director  of  the  Medical  Service  of  the  Hospital;  to  Dr. 
Horatio  B.  Williams,  of  the  Department  of  Physiology,  who  at  all 
times  has  ungrudgingly  placed  his  rare  attainments  as  a  physicist 
and  physiologist  at  the  disposal  of  the  author ;  and  to  his  one-time 
associate  Dr.  Francis  Fraser,  an  acute  observer  and  skilled  clinician. 

The  writer  takes  this  opportunity  to  express  his  thanks  to  the 
Editor  of  The  Archives  of  Diagnosis,  Dr.  Heinrich  Stern,  for  the 
permission  to  utilize  matter  and  illustrations  which  have  appeared 
in  that  journal,  and  his  appreciation  of  the  many  courtesies  of  his 
publishers,  Messrs.  Rebman  and  Company,  extended  while  the 
volume  has  been  passing  through  the  press. 

T.  Stuart  Hart, 
i 60  West  Fifty-ninth  Street,  New  York  City. 


CONTENTS 


Introduction 


PAGE 

CHAPTER  I 


CHAPTER  II 


Anatomy 


Embryonic  heart  of  the  vertebrates :  nodal  tissue :  conducting 
system. 

CHAPTER  III 
Physiology 6 

Neurogenic  theory :  myogenic  theory :  fundamental  properties  of 
myocardial  cells :  stimulus  production :  stimulus  conduction : 
excitability:  contractility:  tonicity:  Bowditch's  law  of  maximal 
contractions  :    refractory  period  :    Stannius'  experiment. 

CHAPTER  IV 
Graphic  Aids  to  Diagnosis 15 

The  polygram  :  the  electrocardiogram  :  normal  curves  :  method 
of  recording:  symbols  used  to  mark  curves:  interpretation  of 
curves. 

CHAPTER  V 

Classification  of  Disturbances  of  Myocardial  Function     26 

Ideal  analysis :  anatomical :  etiological :  clinical :  the  regular 
heart :    the  irregular  heart :    changes  in  rate. 

CHAPTER  VI 
Bradycardia.    Heart  Block 31 

True  bradycardia:  complete  heart  block:  partial  heart  block: 
delayed  conduction  :  pathology  :  etiology  :  identification  :  clinical 
features  :    significance  :    course  :    prognosis. 

CHAPTER  VII 

The  Extrasystole 56 

Pathology:  etiology:  experimental  production:  identification: 
auricular :  nodal :  ventricular  :  four  types  :  interpolated  :  clinical 
significance :    prognosis. 

vii 


Con  n.NTs 


page 


CHAPTER  VIII 

Tachycardia       82 

The  accelerated  heart:  etiology:  pathology:  mechanism:  identi- 
fication:   clinical  significance:    prognosis. 

CHAPTER   IX 

Paroxysmal  Tachycardia 90 

Mechanism:  experimental  production:  pathology:  symptoms: 
identification:      auricular:      ventricular:      clinical     significance: 

prognosis. 

CHAPTER  X 
Auricular  Flutter uy 

Experimental  production:  mechanism:  etiology:  pathology: 
identification:    clinical  course:    significance :    prognosis. 

CHAPTER  XI 
Auricular  Fibrillation 134 

Experimental  production:  mechanism:  pathology:  etiology: 
identification:  polygrams:  electrocardiograms:  clinical  features: 
paroxysmal  fibrillation:  pulse  deficit:  average  systolic  blood 
pressure:    prognosis:    ventricular  fibrillation. 

CHAPTER  XII 
Auricular  Flutter,  Tachycardia  and  Fibrillation      .      .    173 

Relationship:    experimental  production:    clinical  association. 

CHAPTER  XIII 
Alternation        180 

Experimental  production:  mechanism:  pathology:  etiology: 
identification:    clinical   features:    prognosis. 

CHAPTER  XIV 
The  Influence  Exerted  by  the  Extracardial  Nerves  .      .    199 

Anatomy:  physiology:  comparison  of  the  activities  of  the  right 
and  left  vagi :  respiratory  sinus  arrhythmia:  clinical  significance: 
sino-auricular  block:  phasic  variations  of  pulse  rate:  complete 
irregularity  :    clinical  significance. 

CHAPTER  XV 
Mixed  Arrhythmias -'-'-' 

Sinus  arrhythmia  and  defective  conduction:  auricular  fibrilla- 
tion and  extrasystoles :  auricular  lihrillation  and  heart  block: 
heart  block  and  extrasystoles. 


Contents  ix 

PAGE 

CHAPTER  XVT 

Position  of  the  Heart  and  Changes  en  the  Disposition  01 
the  Muscle  Mass 234 

Dextrocardia:  right  ventricular  hypertrophy:  left  ventricular 
hypertrophy. 

CHAPTER  XVII 

Treatment — General  Principles 242 

Individualization:  rest:  exercise:  blood-letting:  diet:  bever- 
ages:   cold  applications:    baths:    spas. 

CHAPTER  XVIII 
Treatment — Drugs 260 

Adrenalin:  alcohol:  ammonia:  atropine:  caffeine:  camphor: 
chloroform  :  digitalis  :  opium  :  the  nitrites  :  pituitary  extracts  : 
strychnine. 

CHAPTER  XIX 
Treatment — Indications  Afforded  by  Types  of  Rhythm   .   276 

Heart  block  :  extrasystoles  :  the  accelerated  heart :  paroxysmal 
tachycardia:  sinus  arrhythmias:  auricular  flutter:  auricular 
fibrillation :    alternation. 

Bibliography       .■.....„•.....  .   306 

Index 314 


ILLUSTRATIONS 


FIGURE 

i.     Diagram:    Conducting  system 


2.  Normal  polygram 

3.  Normal  electrocardiogram    (lead       [.) 

4.  Normal  electrocardiogram    (lead     II.) 

5.  Normal  electrocardiogram    (lead  III.) 

6.  Diagram:  Pressure  changes  in  cardiac  chambers 

7.  Diagram:   Delayed   conduction 

8.  Diagram:    Partial  block    . 

9.  Diagram  :  Complete  block 
10.  Polygram:   Delayed   conduction 
n.  Polygram:  Partial  block 

12.  Polygram :  Complete  block   . 

13.  Polygram:  Delayed  conduction 

14.  Polygram  :  Delayed  conduction 

15.  Polygram:  Partial  block 

16.  Polygram :  Complete  block    . 

17.  Electrocardiogram:  Delayed  conduction 

18.  Electrocardiogram:  Partial   block 

19.  Electrocardiogram :  Partial   block 

20.  Electrocardiogram  :  Complete  block 

21.  Electrocardiogram:  Delayed  conduction 

22.  Electrocardiogram  :  Delayed  conduction 

23.  Electrocardiogram :  Partial  block 

24.  Electrocardiogram :  Partial  block 

25.  Electrocardiogram  :  Complete  block 

26.  Diagram  :  Auricular  extrasystole 

27.  Diagram  :  Auricular  extrasystole 

28.  Diagram :  Ventricular  extrasystole 

29.  Polygram :  Auricular  extrasystole   . 

30.  Polygram :  Auricular  extrasystole   . 

31.  Polygram:  Nodal  extrasystole   . 

32.  Polygram :  Ventricular  extrasystole 

33.  Polygram  :  Pulsus  trigeminus 

34.  Polygram  :  Auricular  and  ventricular  extrasystole 

35.  Electrocardiogram  :  Auricular  extrasystole 

36.  Electrocardiogram  :  Auricular  extrasystole 

37.  Electrocardiogram  :  Auricular  extrasystole 

38.  Electrocardiogram :  Pulsus  trigeminus 

39.  Electrocardiogram  :  Auricular  extrasystole 

40.  Electrocardiogram :  Auricular  extrasystole 

41.  Electrocardiogram :     Ventricular    extrasystole    in    three 

leads 

xi 


PAGE 

5 

'7 
23 
23 
23 
^5 
37 
37 
37 
39 
39 
39 
4i 
4i 
43 
43 
45 
45 
45 
45 
47 
47 
49 
49 
49 
59 
59 
59 
65 
65 
67 
67 
69 

69 

7i 
7i 
7i 
7i 
73 
73 

73 


xii  Illustrations 

FIGURE  PAGE 

42.  Electrocardiogram:  Ventricular  extrasystole  (type  1)     .  7s 

43.  Electrocardiogram:  Ventricular  extrasystole  (type  2)     .  j^, 

44.  Electrocardiogram:  Ventricular  extrasystole  (type  3)     .  j^ 

45.  Electrocardiogram :  Ventricular  extrasystole  (type  4)     .  ~$ 

46.  Electrocardiogram:  Ventricular  extrasystole  .      .     .      .  jy 

47.  Electrocardiogram:  Ventricular  extrasystole  jj 

48.  Electrocardiogram:  Nodal  extrasystole 77 

49.  Electrocardiogram:  Interpolated  extrasystole       .      .      .  79 

50.  Electrocardiogram :  Interpolated  extrasystole       ■      •     •  79 

51.  Electrocardiogram:   Interpolated  extrasystole  7<> 

52.  Electrocardiogram:   Bigeminus 81 

53.  Electrocardiogram:    Ihgeniinus Si 

54.  Electrocardiogram:  Auricular    and    Ventricular    extra- 

systoles      81 

55.  Electrocardiogram:  Ventricular  extrasystoles  (two  types)  81 

56.  Polygram:  Accelerated  heart 87 

57.  Polygram:  Accelerated  heart  (Graves' disease)   ...  87 

58.  Electrocardiogram:   Accelerated  heart 89 

59.  Electrocardiogram:  Accelerated  heart 89 

60.  Diagram :  Auricular  tachycardia 93 

61.  Diagram:  Ventricular  tachycardia    .      .          ....  93 

62.  Polygram:  Auricular  tachycardia  (between  attacks)        .  99 

63.  Polygram:   Auricular  tachycardia 99 

64.  Polygram:  Auricular  extrasystole 101 

65.  Polygram:  Auricular  tachycardia 101 

66.  Polygram:  Auricular  tachycardia 103 

67.  Polygram:   Ventricular  tachycardia 103 

68.  Electrocardiogram:     Auricular     tachycardia       (between 

attacks) ...  105 

69.  Electrocardiogram:  Auricular  tachycardia       ....  105 

70.  Electrocardiogram :     Auricular     tachycardia       (between 

attacks) 107 

71.  Electrocardiogram:  Auricular   tachycardia       ....  107 

72.  Electrocardiogram:     .Auricular     tachycardia       (between 

attacks) 109 

y^-  Electrocardiogram:  Auricular   tachycardia       ....  109 

74.  Electrocardiogram :  Ventricular  extrasystole  .  .      .111 

75.  Electrocardiogram:  Nodal  tachycardia 11 1 

76.  Electrocardiogram:  Paroxysmal  tachycardia  (transition)  113 

77.  Electrocardiogram:  Paroxysmal  tachycardia  ( transition  1  113 

78.  Electrocardiogram:   Paroxysmal  tachycardia  (transition)  113 
7'i.  Electrocardiogram:  Auricular    tachycardia    (transition)  115 

80.  Electrocardiogram:  Ventricular  tachycardia  (transition)  115 

81.  Diagram:  Auricular  flutter 119 


Illustrations  xiii 

FIGURE  PAGE 

82.  Diagram:  Auricular  flutter [19 

83.  Polygram:  Auricular  flutter ui 

84.  Polygram:  Auricular  flutter \2\ 

85.  Electrocardiogram:  Auricular  flutter 123 

86.  Electrocardiogram:  Auricular  flutter 123 

87.  Electrocardiogram:  Auricular  flutter 123 

88.  Electrocardiogram:  Auricular  flutter 125 

89.  Electrocardiogram:  Auricular  flutter 125 

90.  Electrocardiogram:  Auricular  flutter 125 

91.  Electrocardiogram:  Auricular  flutter 127 

92.  Electrocardiogram:  Auricular  flutter 127 

93.  Electrocardiogram:  Auricular  fibrillation         .      .      .      .127 

94.  Electrocardiogram:  Auricular  flutter 129 

95.  Electrocardiogram:  Ventricular  extrasystole   .      .      .      .129 

96.  Electrocardiogram:  Auricular  flutter 131 

97.  Electrocardiogram :  Sequential  rhythm 13] 

98.  Electrocardiogram:  Auricular  fibrillation 131 

99.  Diagram:  Auricular  fibrillation 137 

100.  Diagram:  Age  incidence  of  Auricular  fibrillation       .      .  139 

101.  Sphygmogram :  Auricular  fibrillation 143 

102.  Sphygmogram:  Auricular  fibrillation 143 

103.  Sphygmogram:  Auricular  fibrillation 143 

104.  Sphygmogram:  Auricular  fibrillation 143 

105.  Sphygmogram:  Auricular  fibrillation 143 

106.  Polygram:  Auricular  fibrillation 145 

107.  Polygram:  Auricular  fibrillation      .            145 

108.  Polygram :  Auricular   fibrillation 147 

109.  Polygram :  Auricular  fibrillation 147 

no.  Polygram:  Auricular  fibrillation 149 

in.  Electrocardiogram:  Auricular  fibrillation 151 

112.  Electrocardiogram:  Auricular  fibrillation 151 

113.  Electrocardiogram:  Auricular  fibrillation 153 

114.  Electrocardiogram:  Auricular  fibrillation 153 

115.  Electrocardiogram:  Auricular  fibrillation 155 

116.  Electrocardiogram:  Sinus  rhythm 157 

117.  Electrocardiogram:  Auricular  flutter 157 

118.  Electrocardiogram:   Sinus  rhythm 157 

119.  Electrocardiogram:   Paroxysm    of   Auricular    fibrillation  159 

120.  Electrocardiogram:  Extrasystoles 159 

121.  Electrocardiogram:  Auricular  extrasystole      ....  161 

122.  Electrocardiogram :  Auricular  fibrillation 161 

123.  Electrocardiogram :  Auricular  fibrillation 161 

124.  Diagram:  Pulse  deficit 163 

125.  Electrocardiogram :  Auricular  fibrillation 163 


XIV 


Illustrations 


figure 


PAGE 


[26. 

-7- 

[28. 

[29. 

[30. 

31. 

>3-'- 

[33- 

[34. 
135- 

36. 

^7- 
138. 

139- 

[40. 

[41. 

[42. 

143- 

144. 

'45- 
[46. 
[47. 

[48. 

[49. 
SO- 
51- 

:52- 
53- 
54- 
55- 
56. 

57- 
58. 

59- 

[60. 
161. 
[62. 

[63. 
164. 
165. 
if. 6. 
(67. 
[68. 
[69. 


Electrocardiogram : 
Electrocardiogram ; 
Electrocardiogram : 
Electrocardiogram : 
Electrocardiogram : 
Electrocardiogram : 
Electrocardiogram : 
Electrocardiogram  : 


Diagram :  Pulse  deficit  and  blood  pressure 
Electrocardiogram:  Auricular  fibrillation  . 

Auricular  fibrillation  . 

Auricular  fibrillation  . 

Auricular  fibrillation  . 

Auricular  fibrillation  . 

Auricular  fibrillation   . 

Auricular  fibrillation   . 

Auricular  Butter  and  fibrillati 

Auricular  tachycardia 
Electrocardiogram:  Auricular  flutter    . 
Polygram:  Auricular  Mutter  and  tachycardia  . 

Polygram:  Alternation 

Electrocardiogram :  Alternation        .... 
Polygram:  Alternation  in  tachycardia  . 

Sphygmogram:  Alternation        

Sphygmogram:  Alternation         

Polygram:  Alternation  (apex  and  radial) 

Polygram:  Alternation 

Polygram:  Alternation 

Electrocardiogram :  Alternation        .... 
Electrocardiogram :  Pseudo-alternation 
Electrocardiogram :  Alternation        .... 
Electrocardiogram :  Alternation        .... 
Electrocardiogram :  Tachycardia  and  alternation 
Electrocardiogram:  Tachycardia  and  alternation 
Diagram:  Distribution  of  cardiac  nerves   . 
Electrocardiogram :  Pressure  on  right  vagus  nerve 
Electrocardiogram:  Pressure  on  left  vagus  nerve 
Electrocardiogram :  Right  ocular  pressure 
Electrocardiogram :  Right  ocular  pressure 
Polygram :  Respiratory  sinus  arrhythmia   . 
Polygram:  Respiratory  sinus  arrhythmia   . 
Electrocardiogram :  Respiratory  sinus  arrhythmia 
Electrocardiogram :  Respiratory  sinus  arrhythmia 
Electrocardiogram:  Respiratory  sinus  arrhythmia 
Polygram :  Respiratory  sinus  arrhythmia   . 
Polygram:  Cribber,  Complete  irregularity 
Electrocardiogram :  Dropped  beat    .... 
Electrocardiogram :  Sino-auricular  block    . 
Combined  record:   Sinus  complete  irregularity 
Electrocardiogram:   Sinus  arrhythmia,  phasic 
Electrocardiogram:   Sinus  arrhythmia,  phasic 
Polygram:   Sinus  arrhythmia,  complete  irregularity 


<>5 
[69 
[69 

73 

73 

7? 

75 

75 

7 

77 

77 

79 

[83 

[83 

'85 

[87 

.87 

[89 

[91 

[91 

'93 

'93 

[95 

[95 

197 

197 

201 

203 

203 

205 

205 

207 

207 

209 

209 

21 1 

213 

2 1 3 
215 
215 


21 


217 
217 
219 


Illustrations 


XV 


FIGURE 


170. 
171. 

172. 

173- 

174. 

175- 

176. 
177. 
178. 
179. 
180. 
l8l. 
182. 
183. 
184. 

185. 
186. 
187. 
188. 
189. 
190. 
191. 
192. 

193- 
194. 

195- 

196. 
197. 
198. 
199. 
200. 
201. 
202. 
203. 
204. 
205. 
206. 
207. 
208. 
209. 


irregu 


Electrocardiogram:  .Sinus  arrhythmia,  phasic 
Electrocardiogram:  Sinus  arrhythmia,  complete 

larity 

Electrocardiogram:  Sinus  arrhythmia     and     condu* 

defect  

Electrocardiogram:  Sinus  arrhythmia     and     condu< 

defect         

Electrocardiogram:  Sinus  arrhythmia    variation    in 

ricular  complexes 

Electrocardiogram:   Fibrillation  and  extrasystoles 
Electrocardiogram :   Fibrillation,  block  and  extrasystoles  225 


Polygram  :   Fibrillation,  bloek  and  extrasystoles 
Electrocardiogram :  Auricular  fibrillation  and  block 
Polygram:  Block  and  extrasystoles       .... 
Electrocardiograms :  Block  and  extrasystoles  . 
Electrocardiogram :  Lesion  of  branch  of  His'  bundle 

Polygram :  A-V  bundle  lesion 

Diagram :  Action  currents  of  heart       .... 
Diagram :  Action  currents  of  heart       .... 
Electrocardiogram:  Dextrocardia   (lead      I) 
Electrocardiogram:  Dextrocardia   (lead    II) 
Electrocardiogram:  Dextrocardia   (lead  III) 
Electrocardiogram:  Dextrocardia   (lead  IV) 
Dextrocardia   (lead    V) 
Dextrocardia   (lead  VI) 
Hypertrophy  of  left     ventricle 
Hypertrophy  of  left     ventricle 
Hypertrophy  of  left     ventricle 
Electrocardiogram :  Hypertrophy  of  right  ventricle 
Electrocardiogram :  Hypertrophy  of  right  ventricle 
Electrocardiogram :  Hypertrophy  of  right  ventricle 
Electrocardiogram :  Hypertrophy  of  left     ventricle 
Electrocardiogram :  Hypertrophy  of  left     ventricle 
Electrocardiogram :  Hypertrophy  of  left     ventricle 
Electrocardiogram :  Hypertrophy  of  right  ventricle 
Electrocardiogram:  Hypertrophy  of  right  ventricle 
Electrocardiogram:  Hypertrophy  of  right  ventricle 
Polygram :  Digitalis  effect,  delayed   conduction    . 

Polygram :  Digitalis  effect,  block 

Polygram :  Digitalis  effect,  coupled   rhythm    . 
Electrocardiogram  :  Before  digitalis      .... 
Electrocardiogram:  Digitalis  effect,  sinus  slowing 
Electrocardiogram :  Digitalis  effect,  block 
Electrocardiogram :  Digitalis  effect,  coupled  rhythm 


Electrocardiogram 
Electrocardiogram 
Electrocardiogram 
Electrocardiogram 
Electrocardiogram 


tioi 


PAGE 
22] 

221 

223 

223 

223 

22^ 


227 
22"] 
23I 
23I 

233 

235 
235 
237 
237 
237 
237 
237 
237 
239 
239 
239 
239 
239 
239 
241 

241 
241 
241 
241 
241 
265 
265 
265 
267 
26- 

267 
267 


xvi  Illustrations 

FIGURE  PAGE 

210.  Electrocardiogram:  Digitalis  effect,  coupled  rhythm       .  269 

211.  Electrocardiogram:  Digitalis  effect,  coupled  rhythm       .  269 

212.  Electrocardiogram:   Before  digitalis  (lead      1)    .      .      .  271 

213.  Electrocardiogram:   Before  digitalis  (lead    II)    .      .      .  -71 

214.  Electrocardiogram:   Before  digitalis   (lead  111)  .      .  271 

215.  Electrocardiogram:  After  digitalis,  change   in    T   wave 

(lead      I  )       .     .     . 271 

216.  Electrocardiogram:  After  digitalis,   change   in    T  wave 

( lead    II  ) 271 

217.  Electrocardiogram:  After  digitalis,  change   in    T   wave 

(lead  II  h        .      .      .      .'     .      . 271 

218.  Electrocardiogram:  Block  complete 279 

219.  Electrocardiogram:  After  atropine 279 

220.  Electrocardiogram :   After  atropine 279 

221.  Electrocardiogram:  After  atropine 279 

222.  Electrocardiogram:  Block  complete 28] 

223.  Electrocardiogram:  After  atropine 281 

224.  Electrocardiogram:  After  atropine 281 

225.  Electrocardiogram:  After  atropine 281 

226.  Electrocardiogram:  Auricular  flutter,  right   vagus  pres- 

sure        289 

227 .  Electrocardiogram:  Auricular  flutter,  left      vagus   pres- 

sure        289 

228.  Electrocardiogram:  Auricular  flutter 29] 

22i).  Electrocardiogram:  Auricular  flutter,  digitalis  effect       .  29] 

27,o.  Electrocardiogram:  Auricular  flutter,  digitalis  effect       ■  29] 

231.  Electrocardiogram:  Sinus  rhythm 291 

232.  Sphygmogram:  Auricular  fibrillation 295 

-'33.     Sphygmogram:  Digitalis  effect         295 

234.  Sphygmogram :  Digitalis  effect         295 

235.  Sphygmogram:  Digitalis  effect         2<>^ 

236.  Sphygmogram:    Digitalis  effect          295 

237-     Sphygmogram:  Digitalis  effect         295 

238.  Polygram:  Auricular  fibrillation 297 

239.  Polygram:    Digitalis   effect 2<)J 

240.  Polygram:   Digitalis  effect 297 

241.  Electrocardiogram:  Auricular  fibrillation 299 

242.  Electrocardiogram:  Coupled  rhythm 299 

243.  Electrocardiogram:   Auricular  fibrillation 301 

244.  Electrocardiogram:  Digitalis  effect 301 

245.  Electrocardiogram:  Digitalis  effect 301 

246.  Electrocardiogram:   Digitalis   effect 301 

247.  Diagram:   Pulse  deficit  and  blood  pressure      ....  303 

248.  Diagram:   Pulse  deficit  and  blood  pressure      ....  303 


CHAPTER  I 
Introduction 

The  diagnosis  of  cardiac  abnormalities  requires  a  knowledg 
three  elements:  (i)  Etiological,  (2)  Anatomical  and  (3)  Func- 
tional. In  the  past  while  all  these  features  have  been  considered, 
the  greater  stress  has  been  laid  on  the  anatomical  diagnosis,  etiology 
has  taken  a  somewhat  less  conspicuous  place  and  function  has  per- 
haps received  the  least  attention.  Again  until  recent  years  atten- 
tion has  been  most  closely  directed  to  the  anatomical  abnormalities 
of  the  valves,  the  endocardium  and  the  pericardium,  while  the  myo- 
cardium has  received  relatively  little  clinical  study. 

The  explanation  of  such  a  development  is  perfectly  simple;  our 
methods  of  examining  the  heart  mainly  by  the  employment  of  physi- 
cal signs  were  such  as  to  lend  themselves  particularly  to  the  elucida- 
tion of  the  conditions  of  the  endocardium  and  the  pericardium. 
Reasoning  from  our  physical  signs  we  were  fairly  sure  to  correctly 
interpret  the  kind  and  extent  of  the  damage  to  the  valves  and  the 
pericardium ;  beyond  determining  the  presence  or  absence  of  hyper- 
trophy and  dilatation  our  anatomical  diagnosis  of  the  condition  of 
the  myocardium  was  little  more  than  a  shrewd  guess. 

The  methods  of  cardiac  examination  which  have  been  so  rapidly 
developed  in  the  past  decade  have  afforded  us  the  means  of  studying 
the  heart  from  an  entirely  new  standpoint. 

The  polygraph  and  the  electrocardiograph  have  put  us  in  the  way 
of  studying  many  cardiac  conditions  which  had  hitherto  been  un- 
recognized. These  instruments  afford  us  records  of  the  functional 
activities  of  the  heart;  in  the  main  they  are  records  of  myocardial 
function.  Such  studies  often  permit  us  to  draw  inferences  in  regard 
to  the  anatomical  condition  of  the  heart  muscle.  They  have  already 
helped  us  materially  in  formulating  our  prognosis,  and  our  accuracy 
in  this  regard  should  be  greatly  improved  as  time  passes  and  we 
are  able  to  correlate  our  findings  with  the  events  which  follow  as 
the  years  in  which  such  observations  are  made  increase  in  numbers. 
They  have  furnished  information  which  has  greatly  modified 
our   methods    of    treatment ;    they   should   be    very    useful    in    the 

1 


Introduction 

study  of  the  effect  of  drugs  on  myocardial  function.  Such  records 
are  extremely  valuable  in  that  they  register  graphically  the  func- 
tional condition  and  can  he  preserved  for  future  reference  and  com- 
parison with  later  observations,  unclouded  by  the  haze  with  which 
time  is  so  apt  to  obscure  the  evidence  obtained  by  the  eye,  ear  and 
finger,  even  though  these  are  reinforced  by  carefully  written  notes. 

Perhaps  the  most  important  contribution  which  these  later 
methods  have  made  to  the  average  clinician  is  that  they  have  made 
his  powers  of  observation  more  acute;  they  have  given  new  mean- 
ing to  the  old  physical  signs  and,  with  a  knowledge  of  what  the 
polygram  and  the  electrocardiogram  have  disclosed,  he  is  able  to 
detect  and  interpret  physical  signs  which  hitherto  went  unrecog- 
nized or  were  without  meaning. 

Every  patient  with  abnormal  cardiac  function  cannot  be  brought 
within  the  sphere  of  the  electrical  attachments  of  an  electrocardio- 
graph. The  electrocardiograph  is  an  expensive  laboratory  instru- 
ment suited  to  the  facilities  of  the  large  hospitals  or  the  office  of  the 
consultant  and  cannot  be  included  in  the  armentarium  of  the  aver- 
age general  practitioner.  Even  the  polygraph,  although  portable 
and  not  particularly  expensive  either  in  its  first  cost  or  upkeep,  is 
an  instrument  which  requires  a  certain  amount  of  training  and  a 
very  large  expenditure  of  time  for  its  successful  operation. 

It  is  therefore  comforting  to  know  that  if  one  sufficiently  fa- 
miliarizes himself  with  the  kind  of  evidence  which  these  instruments 
afford,  and  the  nature  of  the  cardiac  abnormalities  upon  which  they 
throw  light,  he  should  by  carefully  cultivating  his  powers  of  ob- 
servation be  able  to  detect  on  physical  examination  the  signs  which 
in  90  per  cent,  of  all  cases  will  allow  him  to  make  as  correct  a  diag- 
nosis and  apply  as  well  a  directed  course  of  treatment  as  he  could 
if  his  observations  were  reinforced  by  the  most  elaborate  records. 


CHAPTER  II 
Anatomy 

In  order  to  elucidate  our  conception  of  the  functional  activities  of 
the  myocardium  it  will  be  well  for  us  to  briefly  review  a  few  ana- 
tomical facts. 

The  embryonic  heart  of  the  vertebrates  first  appears  as  a  tube,  at 
the  posterior  portion  of  which  the  veins  coalesce  to  form  a  cavity 
which  is  known  as  the  sinus  venosus.  In  the  course  of  development 
the  tube  is  bent  upon  itself  and  from  its  wall  a  series  of  chambers 
are  formed  which  ultimately  become  the  auricles  and  ventricles. 
These  features  are  more  clearly  seen  in  some  of  the  lower  verte- 
brates. In  the  higher  vertebrates  the  separation  of  these  chambers 
becomes  less  distinct ;  the  sinus  venosus  disappears  as  a  distinct 
structure  and  is  fused  with  the  tissues  of  the  superior  and  inferior 
cavse  and  that  portion  of  the  right  auricle  which  lies  between  the 
termination  of  these  veins. 

Recent  histological  studies  have  afforded  facts  of  peculiar  interest 
and  lend  support  to  the  theory  of  myocardial  function,  which  is  to- 
day pretty  generally  accepted.  The  study  of  serial  sections  of  the 
mammalian  heart  has  served  to  demonstrate  certain  structures  which 
up  to  this  time  had  been  unrecognized.  Keith  and  Flack  have  de- 
scribed a  collection  of  muscle  cells  of  such  structure  as  to  distin- 
guish them  from  the  surrounding  tissue  lying  near  the  junction  of 
the  superior  cava  with  the  right  auricle  and  extending  along  the 
sulcus  terminalis  for  a  distance  of  about  2  cm.  (in  man).  These 
cells  are  fusiform,  striated,  have  elongated  nuclei  and  are  embedded 
in  dense  connective  tissue ;  they  have  a  special  arterial  supply  and 
intermingled  with  them  are  some  nerve  cells  and  nerve  fibers  which 
connect  with  the  vagal  and  sympathetic  nerve  trunks.  This  special- 
ized tissue  is  known  as  the  sino-auricular  node  and  is  believed  by 
Keith  and  Flack  to  be  a  remnant  of  the  original  sinus  tissue.  Simi- 
lar isolated  masses,  which  are  believed  to  be  remnants  of  the  primi- 
tive canal  as  it  passed  through  the  auricle,  have  been  found  near 
the  coronary  sinus,  in  the  auricular  septum,  in  the  valve  of  Eu- 
stachius  and  at  the  mouths  of  the  pulmonary  veins. 

3 


4  Anatomy 

A  differentiated  mass  of  tissue  similar  in  structure  to  the  sino- 
auricular  noile  and  known  as  the  auriculo-ventricular  node,  was  first 
described  by  Tawara.  It  is  situated  low  down  in  the  auricular  tissue 
at  the  right  posterior  edge  of  the  septum;  at  the  anterior  end  of 
the  auriculo-ventricular  node  these  specialized  muscle  cells  become 
more  parallel  in  arrangement  and  form  a  narrow  band  ensheathed 
in  a  fibrous  canal.  This  structure  is  known  as  the  bundle  of  His. 
It  runs  forward  and  to  the  left  in  the  central  fibrous  portion  of  the 
heart  to  the  membranous  septum  of  the  ventricles;  at  a  point  a  little 
in  front  of  the  anterior  end  of  the  attachment  of  the  median  seg- 
ment of  the  tricuspid  valve  the  bundle  divides  into  two  branches; 
the  left  branch  immediately  passes  through  the  membranous  sep- 
tum and  is  continued  downward  along  the  septum  beneath  the  endo- 
cardium of  the  left  ventricle ;  branches  are  given  off  all  through 
its  course  in  the  septum;  the  principal  branches  going  to  the  papil- 
lary muscles  of  the  mitral  valve;  the  right  branch  of  the  bundle  is 
directed  downward  beneath  the  endocardium  of  the  right  ventricle 
to  the  papillary  muscles  where  subdivisions  begin  to  be  given  off 
from  the  main  trunk. 

The  subdivisions  of  the  conducting  system  are  continued  into  that 
complex  network  lying  beneath  the  endocardium  of  both  ventricles 
known  as  Purkinje's  fibers  and  these  in  turn  make  direct  connection 
with  the  muscle  fibers  of  the  ventricles. 


Anatomy 


Figure  i 

Diagram   of   the   specialized   conducting   system   of    the   heart. 


CH AFTER  III 

Physiology 

As  an  introduction  to  the  study  of  certain  types  of  cardiac  func- 
tion, it  will  be  well  for  us  to  consider  briefly  the  theories  which 
are  at  present  in  vogue  as  to  the  mechanism  of  cardiac  activity, 

THE   NEUROGENIC  THEORY 

Up  to  a  few  years  ago  it  was  generally  held  that  the  origin  and 
regulation  of  the  heart  beat  must  be  located  in  some  part  of  the 
nervous  system.  The  discovery  that  the  contraction  of  the  volun- 
tary muscles  had  its  origin  in  the  central  nervous  system  made  it 
seem  probable  that  the  contraction  of  the  heart  was  the  result  of 
a  stimulus  arising  in  a  nerve  center  which  was  conveyed  to  the 
heart  by  nerve  fibers,  thus  a  musculo-motor  nerve  center  was  as- 
sumed to  exist  and  efforts  were  made  to  locate  it.  When  it  was 
discovered  that  the  excised  heart  of  many  animals,  under  suitable 
conditions,  was  able  to  continue  its  rhythmical  action  for  a  con- 
siderable period,  it  seemed  necessary  to  assume  that  this  motor 
center  was  located  in  the  nervous  substance  embedded  in  the  cardiac 
tissue.  Further,  since  it  was  recognized  that  the  heart  muscle  did 
not  contract  as  a  whole,  but  that  the  activity  was  first  seen  at  the 
sinus  and  thence  spread  successively  over  the  auricles  and  ven- 
tricles, it  was  supposed  that  the  nerve  center  originating  this  stim- 
ulus was  located  in  the  wall  of  the  sinus  and  that  from  this  point 
the  impulses  were  carried  by  the  intrinsic  nerves  of  the  heart  to 
muscle  fibers  of  its  successive  chambers.  The  influence  of  the  vagus 
and  accelerator  nerves  was  recognized  and  their  activity  was  be- 
lieved to  heighten  and  depress  the  automatic  nerve  center  which 
originated  the  rhythmic  contraction  of  the  heart. 

Briefly,  the  "neurogenic  theory"  is  as  follows:  The  initiation  of 
the  rhythmic  activity  of  the  heart  resides  in  an  intra-cardial  nerve 
center,  the  muscle  fibers  respond  to  stimuli  originating  in  this  center, 
the  activities  of  this  nerve  center  are  modified  by  positive  and  nega- 
tive influences  conveyed  to  it  by  the  vagus  and  sympathetic  nerves, 
thus  permitting  an  adjustment  of  the  activity  of  the  heart  in  ac- 

6 


Physiology  7 

cordance  with  the  needs  of  the  body  at  any  particular  moment  by 
a  reflex  mechanism. 

The  important  point  in  which  this  theory  differs  from  the  one 
at  present  generally  accepted  is  that  it  ascribes  to  the  muscle  cells 
an  entirely  passive  role,  making  their  activity  directly  dependent 
on  the  activity  of  the  intra-cardial  nervous  tissue. 

THE   MYOGENIC  THEORY 

As  a  result  of  physiological  investigations  of  the  last  two  decades 
the  theory  of  the  neurogenic  origin  of  the  heart  action  has  been 
opposed  by  the  view  that  the  source  of  the  rhythmical  movement 
is  to  be  found  in  the  heart  muscle  itself.  This  is  known  as  the 
"myogenic  theory."  This  theory  has  been  formulated  to  explain 
and  harmonize  the  facts  discovered  by  the  older  investigators,  such 
as  Bowditch,  Traube  and  Ludwig,  and  the  newer  facts  brought  to 
light  especially  by  the  researches  of  Gaskell  and  Engelmann. 

According  to  this  theory,  the  stimulus  arises  not  in  a  nervous 
center,  but  in  the  muscle  cells  of  the  heart  and  is  conveyed  to 
the  successive  portions  of  the  heart  not  by  the  nerve  fibriles,  but 
by  the  cells  of  the  contractile  tissue  itself. 

The  "myogenic  theory"  is  of  the  highest  importance  in  analyzing 
and  explaining  the  mechanism  of  the  activity  of  the  heart,  and 
affords  us  a  practical  working  hypothesis  of  great  value  in  the 
study  and  treatment  of  pathological  conditions  of  the  myocardium. 

It  will  be  impossible  for  us  to  present  here  the  detailed  evidence 
upon  which  this  theory  is  based.  This  can  be  obtained  from  the 
critical  reviews,  such  as  have  been  written  by  Biederman  and 
Langendorff  (Ergebnisse  der  Physiologie),  and  from  the  original 
papers,  especially  those  of  Engelmann. 

For  our  purpose  it  will  be  sufficient  to  review  briefly  a  few  of 
the  main  facts  upon  which  this  theory  rests. 

The  muscle  cells  of  the  wall  of  the  heart  have  been  found  to 
possess  five  properties,  which,  while  interdependent  to  a  certain 
extent,  are  sufficiently  distinct  to  permit  of  separate  study  and 
description. 

These  five  properties  are : 

1.  Stimulus  production. 

2.  Stimulus  conduction. 


8  Physiology 

3.  Excitability. 

4.  Contractility, 

5.  Tonicity. 

The  cooperation  of  the  first  four  of  these  properties  are  the  means 
through  which  the  rhythmical  movements  of  the  heart  are  initiated 

and  maintained,  and  are  efficient  even  when  the  heart  is  removed 
from  the  body.  In  the  intact  animal  its  needs  at  any  particular 
moment  are  met  by  a  reflex  regulation  through  the  nerves.  The 
influences  thus  brought  to  the  heart  may  affect  any  one  of  these 
five  properties,  and  these  nerve  influences  may  have  a  positive  or 
negative  effect,  heightening  or  depressing-  one  or  more  of  these 
five  properties  of  cardiac  tissue. 

STIM  ULUS    PRODUCTION 

The  nature  of  the  stimulus  which  is  automatically  found  in  the 
cardiac  muscle  cells  is  not  as  yet  definitely  settled.  There  is,  how- 
ever, considerable  evidence  which  indicates  that  it  consists  of  a 
stimulus-material,  a  chemical  compound  the  constituents  of  which 
are  not  as  yet  determined,  but  which  has  definite  affinities  and  is 
governed  by  physico-chemical  laws  the  nature  of  which  we  are 
just  beginning  to  unravel.  It  seems  that  this  stimulus-material  is 
being  continuously  manufactured  and  consists  of  molecules  which 
increase  in  size  and  complexity  until  a  point  is  reached  where  its 
mere  complexity  renders  it  an  unstable  compound,  and  it  is,  there- 
fore, suddenly  decomposed  into  its  constituent  ions.  All  the  stim- 
ulus-material in  existence  at  this  particular  moment  is  destroyed 
by  this  sudden  dissociation,  but  immediately  its  manufacture  is 
recommenced.  This  continuous  formation  of  stimulus-material, 
with  its  automatic  periods  of  dissociation,  constitutes  the  basis  of 
the  rhythmic  stimulation  of  the  heart. 

This  property,  the  manufacture  of  stimulus-material,  is  a  func- 
tion of  the  muscle  cells  of  all  parts  of  the  heart,  but  is  most  highly 
developed  in  the  region  of  the  junction  of  the  superior  cava  of 
the  right  auricle  (the  homologue  of  the  sinus  venosus  of  the  lower 
animals),  hence  the  stimulus  arising  here  sets  the  pace,  under  nor- 
mal conditions,  for  the  rhythmic  activity  of  the  heart,  the  stimulus 
passes  from  the  pacemaker  to  the  successive  portions  of  the  heart, 
and  as  each  muscle  cell  is  stimulated  all  the  stimulus-material  pres- 


Physiology  g 

cut  in  the  cell  at  that  particular  moment  is  dissociated  into  its  con- 
stituent ions. 

Under  certain  pathological  conditions  parts  of  the  heart 
than  the  area  at  the  roots  of  the  great  veins  may  have  this  prop- 
erty (the  construction  of  stimulus-material)  heightened,  and  these 
parts  may,  through  this  process,  become  the  pacemaker  for  the  whole 
heart. 

The  property  of  the  formation  of  stimulus-material  may  be  height- 
ened or  depressed  by  the  influences  brought  to  the  muscle  cells 
by  nerve  influences  and  probably  also  by  variations  in  the  chemical 
constitution  of  the  blood  supply.  Those  influences  which  accelerate 
this  process  are  known  as  positive  chronotropic,  those  which  de- 
press are  known  as  negative  chronotropic. 

EXCITABILITY 

is  that  property  01  the  cardiac  muscle  by  virtue  of  which  it 
responds  to  stimuli.  It  is  probably,  as  Engelmann's  experiments 
show,  quite  distinct  from  the  properties  of  stimulus  produc- 
tion, conduction  and  contractility,  and  is  dependent  upon  mole- 
cules entirely  different  from  those  upon  which  these  other 
depend.  Excitability  may  be  heightened  or  depressed  quite  aside 
from  the  positive  or  negative  changes  which  may  occur  in  the 
other  fundamental  properties.  Excitability  is  measured,  not  by 
the  amount  of  the  reaction  resulting  from  a  stimulus,  but  by  the 
strength  of  the  smallest  stimulus  that  is  sufficient  to  produce  a 
contraction.  Thus  when  a  very  small  stimulus  is  effective  in  pro- 
ducing a  contraction  the  degree  of  excitability  is  high,  when  a  con- 
traction can  be  produced  only  by  a  relatively  large  stimulus  the 
degree  of  excitability  is  low.  Each  contraction  of  the  heart  tem- 
porarily destroys  the  irritability  of  its  muscle  cells.  During  systole 
and  for  a  short  time  after  it  the  heart  cannot  be  excited  even 
by  the  strongest  stimuli.  After  the  systole  the  property  of  ex- 
citability gradually  increases,  and  smaller  and  smaller  stimuli  are 
effective  in  producing  a  contraction.  "When  excitability  is  height- 
ened, it  is  assumed  that  this  is  due  to  a  more  rapid  formation 
of  irritable-material ;  when  it  is  lowered,  it  is  probable  that  the 
irritable-material  is  formed  less  rapidly. 

Nervous  and  nutritional  influences  which  increase  and  diminish 


io  Physiology 

irritability  have  been  named  by  Engelmann  positive  and  negative 
bathmotropic. 

Increase  in  excitability  tends  to  shorten  the  cardiac  cycle,  thus 
increasing  the  rate  and  making  the  heart  susceptible  to  smaller 
stimuli.  Whether  they  he  intrinsic  or  extrinsic,  such  a  change  is 
probably  an  important  predisposing  element  in  the  production  of 
extras\  stoles. 

A  decrease  in  excitability  will  tend  to  lengthen  the  cardiac  cycle 
and,  hence,  will  slow  the  heart. 

CONDUCTIVITY 

Formerly  it  was  believed  that  the  conduction  of  stimuli  to 
successive  portions  of  the  heart  was  a  function  which  helonged 
exclusively  to  the  intrinsic  nerves  of  the  heart  wall.  To-day 
the  evidence  is  very  strong  that  the  function  of  conducting 
stimuli  is  a  property  of  the  muscle  cells  of  the  heart  wall.  Without 
attempting  to  give  all  the  evidence  upon  which  the  latter  assump- 
tion rests,  we  may  mention  the  following  facts:  Morphological  and 
embryological  evidence  lend  probability  to  the  theory  that  the  heart 
muscle  cells  are  capable  of  transmitting  stimuli  from  muscle  cell 
to  muscle  cell.  Experimentally  the  wave  of  conduction  can  be  made 
to  start  from  any  point  in  the  wall  of  the  heart  and  pass  in  a 
direction  opposite  to  that  which  it  normally  takes.  This  would  be 
exceedingly  difficult  to  explain  on  the  assumption  that  conduction 
is  dependent  on  a  reflex  nervous  mechanism,  while  the  hypothesis 
which  assigns  this  to  the  muscle  cell  renders  this  phenomenon  quite 
intelligible. 

The  rate  of  conduction  in  the  heart  is  relatively  slow.  In  the 
frog's  heart  (according  to  Engelmann)  it  is  three  hundred  times 
slower  than  in  motor  nerves,  and  the  rate  of  conduction  from 
auricle  to  ventricle,  where  connection  is  made  by  a  very  narrow 
strip  of  muscle,  the  conduction  is  even   slower. 

Conductivity  is  temporarily  destroyed  during  the  systole  of  the 
heart,  but  returns  gradually  after  each  contraction;  hence,  this 
property  is  believed  to  be  dependent  upon  molecules  wdiich  on 
stimulation  are  broken  down  into  their  constituent  ions,  whence 
they  are  gradually  rebuilt,  becoming  less  stable  as  the  molecule 
increases  in  size. 


Physiology  ii 

Conductivity  can  be  heightened  and  depressed  by  nervous  influ- 
ences by  the  application  of  heat  and  cold  and  the  employment 
of  chemicals  which  modify  the  normal  metabolism.  It  is  slowed 
or  abolished  by  mechanically  narrowing  the  muscle  mass.  Such 
influences  are  termed  positive  and  negative  dromotropic  effects. 

CONTRACTILITY 

is  that  property  by  virtue  of  which  the  muscle  cells  become  short- 
ened, thus  narrowing  the  chambers  of  the  heart  and  emptying  them 
of  their  contents.  Since,  in  accordance  with  the  law  established 
by  Bowditch,  the  contractions  of  the  heart  are  always  maximal, 
i.e.,  if  it  contracts  at  all,  it  contracts  with  all  the  power  of  which 
it  is  capable  at  the  particular  moment.  The  size  of  the  contraction 
is  a  measure  of  its  contractility. 

The  property  of  contractility,  as  is  the  case  with  the  other  funda- 
mental properties,  is  destroyed  for  the  time  being  by  the  contrac- 
tion of  the  muscle  cell,  and,  as  is  the  case  with  the  others,  this 
function  is  gradually  restored  during  systole.  The  contractile  power, 
therefore,  varies  with  the  length  of  the  diastole ;  that  is  to  say,  the 
longer  the  period  allowed  for  recuperation,  the  greater  will  be  the 
power  of  the  succeeding  contraction. 

Nervous  and  nutritional  influences  which  heighten  or  depress  con- 
tractility are  termed  positive  and  negative  inotropic  effects,  re- 
spectively. 

While  the  functions  of  stimulus  production,  excitability,  con- 
ductivity and  contractility  can  be  shown  to  be  distinct  properties 
of  cardiac  muscle,  their  interdependence  is  well  illustrated  by  the 
effect  which  a  modification  of  one  or  more  of  these  may  have 
upon  contractility.  For  example,  any  considerable  increase  in  the 
properties  of  stimulus  formation  and  excitability  have  a  negative 
inotropic  effect  and  contractions  are  less  powerful,  while  a  de- 
pression of  stimulus  production  and  excitability  have  a  positive 
inotropic  effect  and  contractility  is  increased. 

TONICITY 

Every  muscle  normally  possesses  a  certain  tone ;  that  is  to  say, 
even  when  it  is  not  contracting  it  maintains  a  position  which  is 


[2  Physiology 

somewhat  short  of  complete  relaxation.  The  muscle  of  the  heart 
is  no  exception  in  this  general  rule. 

Tonus,  while  related  to  the  other  fundamental  properties  of 
heart  muscle,  is  probably  quite  distinct  from  them;  for  example, 
Porter*  has  shown  that,  unlike  the  other  fundamental  properties, 
"tonus  contractions"  are  proportional  to  the  strength  of  the  stim- 
ulus employed  and  have  no  refractory  period.  In  the  frog,  Ilolf- 
mannt  was  able  to  demonstrate  that  stimulation  of  certain  vagus 
fibers  increase  the  size  and  force  of  the  contractions  of  the 
heart  and  increase  its  tonicity  without  modifying  the  cardiac 
rate. 

Tonus  allows  the  heart  wall  to  resist  stretching  during  diastole. 
The  force  which  stretches  the  heart  during  diastole  is  the  pressure 
of  the  blood  flowing  from  the  great  veins.  This  flow  will  continue 
until  an  equilibrium  is  established  between  venous  pressure  and 
the  tonicity  of  the  heart. 

A  normal  tone  aids  in  maintaining  the  efficiency  of  the  heart 
(i)  by  resisting  over-filling,  and  (2)  by  promoting  an  initial  ten- 
sion which  is  favorable  to  an  effective  contraction.  Changes  in 
tone  are  essential  in  order  that  the  ventricles  may  be  capable  of 
receiving  varying  quantities  of  blood,  but  an  excessive  tone  may 
lead  to  a  ventricular  capacity  which  is  too  small  and  a  diminished 
tone  may  admit  too  large  a  volume  of  blood  and,  therefore,  lead 
to  dilatation  and  an  inefficient  emptying  of  the  ventricles. 

The  relation  of  tonus  to  dilatation  and  cardiac  insufficiency  in 
the  individual  case  is  obscure  and  is  a  subject  which  requires 
further  careful  investigation. 

In  order  to  intelligently  interpret  the  myocardial  activities  sev- 
eral other  features  should  be  held  prominently  in  mind.  The  law 
of  "All  or  None"  or  of  "Maximal  Contractions"  was  discovered  by 
Bowditch  in  1871.  lie  showed  that  if  a  stimulus  was  strong  enough 
to  induce  a  contraction,  the  cardiac  muscle  responded  to  that  stimu- 
lus with  all  the  contractile  power  of  which  it  was  capable  at  that 
particular  moment ;  also  that  the  size  of  the  contraction  was  inde- 
pendent of  the  strength  of  the  exciting  stimulus;  a  small  stimulus, 
if  effective,  produced  a  contraction  just  as  large  as  a  stronger  stimu- 

*Amer.   Jour.    Physiol.,    1906,  xv,    I. 
"rArch.   f.  d.  ges.   Physiol.,   1895,  lx,  139. 


Physiology  13 

lus.    When  the  heart  muscle  was  stimulated  it  responded  with  a 
maximal  contraction  or  none  at  all. 

That  the  cardiac  muscle  cells  possess  a  "Refractory  Period"  was 
discovered  by  Marey  in  1875.  lie  was  able  to  show  that  there  was 
a  period  beginning  just  before  systole  and  continuing  a  short  time 
after  it  during  which  the  heart  will  not  respond  to  stimuli  even  if 
these  are  of  great  strength.  The  studies  of  Engelmann  have  demon- 
strated that  during  the  refractory  period  the  properties  of  excita- 
bility, conduction  and  contractility  arc  all  abolished.  After  systole 
excitability  is  gradually  restored  so  that,  whereas  immediately  after 
the  refractory  period  the  heart  will  respond  only  to  stimuli  of  great 
strength,  as  diastole  advances  the  minimal  stimulus  necessary  to  pro- 
duce a  contraction  becomes  progressively  smaller.  Engelmann 
showed  in  like  manner  that  the  conductivity  and  contractility  grad- 
ually increased  with  the  lengthening  of  the  time  between  the  end 
of  the  refractory  period  and  the  time  when  the  stimulus  was  applied. 

When  we  come  to  study  the  functions  of  the  primitive  cardiac 
tube  in  the  lower  vertebrates  (as  for  example  the  frog,  in  which 
portions  of  the  primitive  tube  still  exist,  as  the  sinus  venosus,  au- 
ricular canal  and  the  aortic  bulb),  we  find  that  all  of  its  parts  pos- 
sess in  a  high  degree  the  power  of  originating  stimuli,  but  the  pos- 
terior portion  of  the  tube  as  represented  by  the  sinus  venosus  is  even 
more  excitable  than  the  other  parts  of  the  tube,  hence  normally  the 
cardiac  contractions  start  from  the  sinus. 

The  capability  of  parts  of  the  frog's  heart,  ether  than  the  sinus, 
to  originate  stimuli  resulting  in  contraction,  is  demonstrated  by  the 
Stannius  experiment.  When  a  ligature  is  so  applied  as  to  separate 
the  sinus  venosus  from  the  auricle,  the  sinus  will  continue  to  con- 
tract rhythmically,  but  the  rest  of  the  heart  ceases  to  move ;  after 
a  time,  however,  the  auricle  and  ventricle  again  begin  to  beat,  but 
at  a  rate  slower  than  that  of  the  sinus  and  quite  independent  of  the 
sinus  rhythm.  If  now  a  second  ligature  be  applied  between  the 
auricle  and  the  ventricle,  the  auricle  will  continue  to  beat  and  after 
a  short  pause  the  ventricle  will  begin  to  contract  rhythmically  at  a 
rate  slower  than  that  of  the  auricle  and  independent  both  of  the 
sinus  and  of  the  auricle. 

There  are  several  phenomena  presented  in  this  experiment  which 
particularly  attract  our  attention. 


14  Physiology 

i.  The  capacity  of  each  chamber  to  initiate  rhythmic  contractions 
independent  of  the  other  parts  of  the  heart. 

2.  The  rate  of  the  spontaneous  rhythmic  contractions  is  fastest 
for  the  sinus,  intermediate  fur  the  auricle,  slowest  for  the  ventricle. 

}.  In  the  intact  heart,  before  such  ligatures  arc  applied,  the  rate 
of  the  rhythmic  contractions  of  the  whole  organ  is  determined  by 
the  rate  of  the  sinus,  i.e.,  by  the  portion  which  has  the  fastest 
rate,  or,  in  other  words,  that  which  has  the  greatest  excitability. 
In  a  similar  manner,  when  the  sinus  is  cut  oli",  the  auricle  sets  the 
pace  for  the  ventricle. 

As  was  pointed  out  in  the  preceding  section  on  the  histology  of 
the  mammalian  heart  certain  special  structures  have  been  found  in 
different  portions  of  the  heart  which  have  many  features  in  com- 
mon. These  are  the  "Sinus  Node,"  the  "Auriculo-voitricular 
Node"  and  the  "Bundle  of  His."  A  study  of  the  functions  of  these 
structures  leads  us  to  believe  that  they  are  remnants  of  the  primi- 
tive cardiac  tube  and  retain  the  qualities  of  the  original  tube  in  a 
higher  degree  than  other  portions  of  the  cardiac  musculature. 

Anatomical,  morphological  and  developmental  evidence  indicate 
that  the  "Sinus  Node"  is  the  normal  pacemaker  of  the  mammalian 
heart.  This  evidence  has  been  reinforced  by  considerable  experi- 
mental work,  a  brief  digest  of  which  may  be  found  in  Thomas 
Lewis'  valuable  work,  "The  Mechanism  of  the  Heart  Beat,"  Chap- 
ter IV. 

There  is  certain  evidence  that  under  pathological  conditions  the 
"Auriculo-ventricular  Node"  may  become  the  pacemaker  of  the 
heart,  giving  rise  to  a  form  of  heart  activity  that  is  known  as  "Nodal 
Rhythm." 

In  other  pathological  conditions  when  the  conducting  path  from 
the  auricle  to  the  ventricle  is  severed  (termed  auriculo-ventricular 
block),  the  evidence  is  in  favor  of  the  assumption  that  the  main 
trunk  or  one  of  the  branches  of  the  "Bundle  of  His"  originates  the 
stimuli  which  set  the  pace  for  the  ideo-ventricular  rhythm  which  is 
then  established. 


CHAPTER  IV 
Graphic  Aids  to  Diagnosis 

Two  of  the  aids  which  have  of  late  been  extensively  utilized  to 
interpret  myocardial  function  arc  the  polygram  and  the  electro- 
cardiogram. The  polygram  is  a  graphic,  synchronous  record  of 
two  or  more  parts  of  the  circulatory  system,  usually  of  the  radial 
and  jugular  pulses.  The  main  facts  of  clinical  importance  which 
have  been  obtained  from  polygraphic  studies  of  the  circulation  have 
been  derived  from  a  comparison  of  the  relations  of  the  auricular 
and  ventricular  activities.  The  value  of  records  of  the  apex  beat, 
carotid,  brachial  and  radial  arteries,  depends  on  the  fact  that  they 
represent  more  or  less  accurately  the  activities  of  the  left  ventricle, 
while  the  movements  of  the  jugular  veins  or  pulsating  liver  give  us 
a  certain  insight  into  the  activities  of  the  right  auricle. 

In  clinical  work  we  usually  make  use  of  synchronous  records  of 
the  radial  and  jugular  tracings  (Figure  2).  The  principal  waves  of 
the  jugular  tracings  are,  the  wave  of  auricular  systole  (a)  ;  the 
wave  synchronous  with,  and  probably  due  to  carotid  pulsation  (c)  ; 
the  (v)  wave,  due  to  rising  auricular  pressure  during  the  ventricu- 
lar systole ;  the  depression  (x)  is  mainly  due  to  the  relaxation  of  the 
auricle  after  its  systole;  the  depression  (y)  is  due  to  emptying  of 
the  auricle  after  the  opening  of  the  tricuspid  valve ;  the  closure  of 
the  semi-lunar  valve  is  frequently  marked  by  a  notch  in  the  ascend- 
ing limb  of  the  (v)  wave,  and  the  two  portions  of  the  wave  have 
been  designated  (z^s)  and  (z,d)  (Rihl),  to  indicate  their  relations  to 
systole  and  diastole.  The  opening  of  the  tricuspid  valve  is  indicated 
by  the  termination  of  the  (v)  wave. 

A  fourth  wave,  which  sometimes  appears  in  diastole  and  called 
the  (h)  wave  (Gibson),  is  believed  to  mark  the  closure  of  the 
auriculo-ventricular  valves. 

The  first  step  necessary  in  analyzing  the  jugular  tracing  is  to 
locate  the  (c)  wave.  To  accomplish  this  one  measures  accurately 
with  dividers  the  distance  of  the  foot  point  of  any  given  radial 
wave  from  the  line  marking  the  beginning  of  the  radial  tracing. 
One  then  measures  oft"  the  corresponding  distance  from  the  start- 


a 


16  Graphic  Aids  to  Diagnosis 

ing  place  oi  the  jugular  tracing;  at  the  distance  equivalent  to  o.i 

md  preceding  this  point  will  be  found  the  (c)  wave,  since  the 

pulse  wave  requires  o.i  second  to  travel  from  the  carotid  to  the 

radial  at  the  wrist.  In  the  normal  tracing  the  (a)  wave  will  he 
found  preceding  the  (c)  wave  by  0.2  second.  'The  {■:■)  wave  fol- 
lows the  (c)  wave,  separated  from  it  hy  the  depression  (.r).    The 

depression  (y)   follows  the  (y)   wave. 

In  various  arrhythmic  conditions  of  the  heart  there  will  he  found 
variations  in  the  relations  of  these  waves  of  the  jugular  pulse. 
These  variations  afford  us  the  means  of  determining  the  time  re- 
lations of  the  auricular  and  ventricular  activities,  and  from  these  can 
be  deduced  certain  abnormalities  in  the  fundamental  properties  of 
the  cardiac  tissues. 

Much  time  and  annoyance  in  taking  polygrams  may  be  saved 
if  one  systematically  pays  attention  to  the  following  apparently  in- 
significant details.  One  should  always  first  examine  his  instrument 
to  see  if  all  parts,  particularly  the  tambours,  are  in  good  working 
order;  the  clockwork  (usually  two  sets)  should  be  wound.  If 
smoked  paper  is  to  be  used,  an  ample  supply  should  be  prepared, 
so  that  one  need  not  interrupt  his  work  for  this  purpose  during 
the  record-taking  period.  For  smoking  the  paper  a  large  candle, 
a  kerosene  lamp,  burning  camphor  or  a  gas  burner  fitted  with  a 
fantail  may  he  employed. 

Personally  I  prefer  the  gas  burner  when  practical,  as  by  this 
means  the  smoke  is  laid  on  the  paper  more  evenly  and  less  heavily 
than  by  the  other  methods.  If  the  ink  polygraph  is  used,  the  pens 
should  be  carefully  cleaned  and  filled  with  the  writing  fluid. 

The  patient  should  be  placed  on  a  couch  or  bed  with  clothing 
loosened,  to  allow  access  to  the  parts  which  it  is  wished  to  in- 
vestigate. He  should  be  in  a  comfortable  position,  so  that  he  may 
relax  and  lie  quietly.  In  taking  a  record  of  the  jugular  pulse,  the 
shoulders  should  be  slightly  raised,  the  head  somewhat  flexed  for- 
ward and  rotated  to  the  right  and  supported  by  pillows  so  that  the 
sternocleidomastoid  muscles  may  be  perfectly  relaxed.  When  a 
radial  tracing  is  taken,  the  position  of  the  radial  artery  should  be 
marked  with  a  skin  pencil ;  this  will  be  found  to  facilitate  greatly 
the  correct  adjustment  of  the  spring  of  the  instrument  over  the 
radial  artery.     The  spring  of  the  instrument  should  rest  immedi- 


Graphic  Aids  to  Diagnosis 


U 


Figure  2.    Normal  Polygram 

1,  beginning  of  auricular  contraction;  2,  beginning  of  apex  beat;  3,  beginning  of 
carotid  wave;  4,  beginning  of  radial  wave;  5,  closure  of  semi-lunar  valves;  6,  opening 
of   tricuspid   valve;    E  =  3  -  5  =  ventricular  systolic   period. 


i8  Graphic  Aids  to  Diagnosis 

atcly  over  the  artery  to  avoid  distortion  of  the  form  of  the  pulse 
tracing,  which  a  lateral  displacement  may  cause.     If  the  pressure 

of  the  spring  on  the  arterial  wall  is  equivalent  to  the  diastolic  pres- 
sure of  the  patient,  the  movements  of  the  spring  will  he  maximal; 
if  this  gives  a  movement  to  the  writing  lever  greater  than  is  de- 
sired, the  excursions  may  he  reduced  by  slightly  increasing  or  dimin- 
ishing the  pressure  of  the  spring.  (  In  polygraph  work  the  time  rela- 
tions of  the  various  tracings  are  usually  of  greater  importance  than 
the  size  of  the  various  waves. )  In  adjusting  the  brachial  cuff  of 
the  Uskoff  or  Erlanger  apparatus,  the  pressure  is  usually  raised 
to  a  point  equivalent  to  the  patient's  diastolic  pressure.  ( In  using 
this  instrument  one  sometimes  meets  with  difficulty  in  securing  a 
sharp  "footpoint"  for  the  waves  of  the  brachial  record.)  The  re- 
ceiving apparatus  for  an  apex  tracing  may  he  a  small  Mackenzie 
cup  or  one  of  the  more  elahorate  forms  of  the  so-called  "cardio- 
graphs," which  may  he  strapped  to  the  chest  wall  or  held  by  an 
assistant.  The  position  of  the  apex  thrust  should  he  marked  with 
a  skin  pencil  and  care  should  be  taken  to  adjust  the  receiver  to 
this  point.  (A  receiver  placed  inside  the  apex  beat  will  often  record 
the  systolic  retraction  of  the  tissues  near  the  apex,  giving  the  so- 
called  "inverted  cardiogram.")  The  jugular  tracings  are  best  taken 
with  a  Mackenzie  cup  about  one  and  one-half  inches  in  diameter 
and  slightly  flattened  on  one  edge.  The  cup  is  placed  over  the 
jugular  bulb,  just  above  and  about  one-half  inch  to  the  right  of 
the  right  sternoclavicular  junction.  The  flattened  edge  of  the  cup 
should  be  parallel  to  the  upper  border  of  the  clavicle  and  should 
be  held  gently  in  position  by  the  operator's  hand,  which  is  steadied 
by  resting  lightly  on  the  chest  wall ;  the  cup  is  provided  with  a 
pin-hole  vent,  which  may  be  covered  by  the  operator's  finger,  who 
can  thus  adjust  the  internal  air  pressure  without  removing  the 
cup.  Any  considerable  pressure  of  the  cup  over  the  veins  must 
be  avoided.  The  receiving  cup  may  be  shifted  about  to  obtain  the 
point  of  maximum  venous  pulsation ;  at  times  the  best  tracings 
are  obtained  at  a  point  higher  up  on  the  neck. 

In  taking  tracings  of  the  movements  of  the  liver,  a  larger  cup 
with  a  flattened  edge  should  be  employed  ;  the  abdomen  should  be 
relaxed  and  the  cup  brought  in  contact  with  the  under  surface 
of  the  liver. 


Graphic  Aids  to  Diagnosis 


J  <J 


Records  of  the  left  auricle  have  been  taken  by  introducing  into 
the  esophagus  a  stomach  tube  with  a  single  lateral  opening  covered 
with  a  delicate  rubber  membrane.  The  tube  must  be  introduced 
to  a  point  which  brings  the  rubber  membrane  opposite  the  pulsating 
auricle.  In  taking  such  records  a  preliminary  course  of  training 
is  necessary  to  accustom  the  patient  to  the  use  of  the  tube. 

The  changes  in  air  pressure  produced  in  the  various  receiving 
devices  are  transmitted  to  the  tambours  connected  with  the  writing 
levers  by  rubber  tubing;  each  of  these  tubes  should  be  provided 
with  a  small  lateral  valve  closed  automatically  by  a  spring  which 
can  be  released  at  any  time  to  regulate  the  internal  air  pressure. 

When  all  the  levers  are  seen  to  be  correctly  adjusted  and  moving 
freely,  the  time  marker  is  started  and  finally  the  clockwork  moving 
the  paper.  At  times,  when  the  respiratory  movements  distort  the 
jugular  tracing,  it  will  be  found  of  advantage  to  have  the  patient 
hold  his  breath  while  the  polygram  is  being  taken.  From  time  to 
time  the  paper  should  be  stopped  so  that  synchronous  points  on  the 
various  curves  may  be  indicated  for  the  sake  of  subsequent  meas- 
urement. The  smoked  paper  records  are  fixed  by  passing  them 
through   a   bath   of   varnish. 

The  electrocardiograph  records  the  differences  in  electrical  poten- 
tial of  the  heart  muscle  during  its  activity.  That  every  contrac- 
tion of  a  muscle  is  accompanied  by  certain  definite  changes  in 
electrical  potential  has  been  known  since  1856,  when  Kolliker  and 
Miiller  detected  the  action  current  of  the  frog's  heart  by  applying 
electrodes  to  its  surface.  When  a  wave  of  contraction  passes  over 
a  muscle,  that  portion  of  the  muscle  which  is  actively  contracting 
is  electrically  negative  to  all  other  parts  of  the  muscle.  It  is  the 
object  of  electrocardiography  to  detect  those  differences  of  poten- 
tial which  occur  during  the  contraction  of  the  heart  muscle  and 
to  record  them  graphically.  This  has  been  made  possible  clinically 
by  the  genius  of  Professor  Einthoven,  of  Leyden,  to  whom  we  are 
indebted  for  the  construction  of  an  exceedingly  delicate  gal- 
vanometer known  as  Einthovens  String  Galvanometer.  This  in- 
strument consists  of  a  powerful  electromagnet  activated  by  a  storage 
battery  of  five  to  six  amperes  furnishing  about  ten  volts.  Between 
the  poles  of  this  electro-magnet  is  stretched  a  delicate  filament  of 
platinum  or  of  silvered  quartz;  the  diameter  of  one  of  these  threads 


20  Graphic  Aids  to  Diagnosis 

is  from  two  to  four  micron?  (about  half  the  diameter  of  .1  red 
blood-corpuscle)  and  their  resistance  is  about  5,000  ohms.  When 
a  current  of  electricity  passes  through  this  string,  at  right  angles 
to  the  lines  of  force  of  the  magnetic  field  of  the  electro-magnet,  the 
string  is  deflected  to  one  side  or  the  other,  according  to  the  direc- 
tion in  which  the  current  passes.  An  arc  light  passing  through  a 
system  of  condensing  lenses  and  Zeiss  objective  and  projection  ocu- 
lars, magnifies  and  focusses  the  shadow  of  the  string  on  a  photo- 
graphic plate  or  film. 

A  Weston  normal  element,  furnishing  one  volt  in  connection  with 
a  rheostat,  is  so  arranged  that  the  operator  may  send  any  desired 
fraction  of  this  current  through  the  string  in  either  direction,  and 
thus  determine  the  sensitiveness  of  the  instrument  at  any  particular 
moment.  The  tension  of  the  string  may  be  increased  or  dimin- 
ished at  will  by  means  of  a  micrometer  screw,  thus  readily  varying 
its  sensitiveness.  The  string  is  usually  adjusted  so  that  the  pas- 
sage of  one  millivolt  of  current  causes  a  deflection  of  the  shadow 
of  one  centimeter,  ddiis  has  been  the  standard  used  in  the  records 
presented  in  this  entire  book. 

When  a  patient  is  placed  in  the  galvanometer  circuit  by  attach- 
ing suitable  electrodes  to  the  surface  of  the  body,  it  is  found  that 
certain  differences  of  potential  are  present  which  cause  a  deflec- 
tion of  the  string  (the  so-called  "skin  current,"  probably  due  to 
the  glandular  activities  of  the  body).  In  order  that  the  delicate 
differences  of  potential  of  cardiac  activity  may  not  be  obscured  by 
this  "skin  current,"  it  is  neutralized  by  introducing  into  the  cir- 
cuit in  the  opposite  direction,  by  means  of  a  rheostat,  a  sufficient 
portion  of  the  current  from  a  single  dry  battery  cell  to  exactly 
counterbalance  the  "skin  current." 

For  the  purpose  of  enclosing  the  patient  in  the  circuit,  various 
forms  of  electrodes  are  employed,  usually  metal  vessels  containing 
solutions  of  common  salt,  in  which  the  extremities  are  immersed. 
A  more  satisfactory  electrode  devised  by  Dr.  11.  B.  Williams  is 
used  in  our  work  at  the  Presbyterian  Hospital.  It  consists  of  a 
large  thin  flexible  sheet  of  German  silver ;  this  is  moistened  with 
hot  salt  solution  and  bandaged  to  the  extremities  with  flannel  strips. 

A  Jacquet  timer,  recording  fifths  of  a  second,  is  placed  in  front 
of  the  camera  so  that  the  time  intervals  are  recorded  simultaneously 


Graphic  Aids  to  Diagnosis  21 

with  the  movements  of  the  string.  The  photographic  .npparnt us 
which  we  have  employed  makes  use  of  a  200-foot  kodak  film  moved 
by  an  electric  motor,  with  convenient  devices  for  numbering,  ex- 
posing, cutting  off,  and  removing  the  film  according  to  the  length 
desired.  In  the  Presbyterian  Hospital  wires  are  run  from  the 
laboratory  to  the  several  wards,  so  that  records  are  easily  taken 
of  patients  without  removing  them  from  their  beds.  Records  thus 
taken  at  a  distance  are  known  as  tclccardiograms. 

The  patient  under  observation  should  be  warm,  relaxed  and  per- 
fectly quiet,  since  tenseness  of  the  muscles,  muscular  movements, 
shivering,  talking,  coughing,  etc.,  cause  irregular  movements  of  the 
string.  (These,  however,  are  usually  easily  differentiated  from  the 
movements  due  to  heart  activity.) 

The  steps  necessary  to  be  taken  in  making  an  electrocardiogram 
arc  as  follows : 

1.  Attachment  of  three  electrodes  to  the  patient  (right  arm,  left 
arm  and  left  leg). 

2.  The  estimation  of  the  resistance  in  each  of  the  three  leads. 

3.  The   standardization   of   the   galvanometer. 

4.  The  compensation  of  the  "skin  current." 

5.  The  recording  of  the  movements  of  the  string  of  the  gal- 
vanometer under  the  influence  of  the  heart  action. 

6.  The  development  and  printing  of  the  films. 

When  no  current  is  passing  through  the  string  of  the  galvano- 
meter the  electrocardiogram  represents  a  base  line  which  shows  the 
string  at  rest.  When  the  current  passes  through  the  string  it  is  de- 
flected and  these  deflections  are  shown  in  the  electrocardiogram  as 
waves  varying  in  height  and  length.  The  principal  features  of  the 
lettering  of  the  waves  of  the  normal  electrocardiogram,  as  first  sug- 
gested by  Einthoven,  are  shown  in  Figures  3,  4,  5.  The  wave  (P) 
corresponds  to  the  systole  of  the  auricles;  the  waves  (0,  R,  S,  T) 
correspond  to  the  systole  of  the  ventricles;  of  these  waves  (R)  and 
(T)  are  most  constant  and  are  best  understood.  (0)  and  (S)  may 
either  one  or  both  be  absent  in  the  electrocardiogram  of  the  healthy 
subject.  A  satisfactory  interpretation  of  all  of  the  elements  of  the 
electrocardiogram  is  not  yet  possible,  but  the  following  summary 
indicates  the  significance  of  the  main  features  as  most  generally  ac- 


22  Graphic  Aids  xo  Diagnosis 

ceptcd  at  the  present  time:      (Some  interpretations  less  generally 
accepted   are   placed    in    brackets.) 

P  =  The  auricular  systole.  (Conduction  through  the  auricle  or 
activity  of  the  sinus  region  plus  conduction  through  the 
auricle.  | 

P  to  R  =  The  time  occupied  in  the  conduction  of  the  impulse  from 
the  auricle  to  the  ventricle,  normally  O.I2  to  0.17  second. 

Q  =  The  first  evidence  of  ventricular  activity  ;  probably  portions  of 
the  ventricular  muscle  at  some  distance  from  the  base. 

R  =  The  activity  of  the  basal  portions  of  both  ventricles.  (Impulse 
conduction   from  base  to  apex.) 

S  =  Activity  of  apical  portion  of  both  ventricles.  (Impulse  con- 
duction from  apex  to  base.) 

S-T  =  A  balance  of  the  potential  between  base  and  apex.  (An 
absence  of  conduction.) 

T  =  The  final  activity  of  the  ventricle ;  probably  the  basal  portion 
near  the  roots  of  the  great  arteries.  (Change  of  elec- 
trical potential  accompanying  contraction  of  the  whole 
ventricle.) 

T  to  the  following  P  —  The  diastolic  period  when  no  current  is 
being  developed. 

U  =  The  relaxation  of  the  ventricles.  (Electrical  variation  of  the 
arteries.) 

In  general  it  may  be  said  that  there  are  two  views  as  to  the 
activities  which  produce  the  differences  in  electrical  potential:  (1) 
that  all  the  waves  accompany  the  excitation  process;  (2)  that  a 
part  of  the  waves  are  due  to  excitation  or  conduction  and  the 
remainder  accompany  the  activity  of  contraction. 

Sufficient  evidence  to  make  a  decision  between  these  views  is  not 
yet  at  hand. 

The  character  of  the  electrocardiographic  curve  varies  with  the 
parts  of  the  body  from  which  it  is  derived.  In  routine  work  it  is 
customary  to  take  three  records  from  each  patient  designated  as 
follows : 


Graphic  Aids  to  Diagnosis 
Normal  Electrocardiogram 


23 


■  .    ',. 

--'     ■ 

n 

1                 1 

T>            t                T 

■"  ■■»    11   nrA                |>      ^           .     (1     ,^h                 ll       -«.                 li      j^ 

BftB^^Mllilljil^iwiiilW^Bn 

~ 

^ 

■$ 

-t-:   --t---iL- 

_'w. 

nJtanA 

Figure  3 

Lead  I  (right  arm — left  arm) 


Figure  4 

Lead  II  (right  arm — left  leg) 


Figure  5 

Lead  III  (left  arm— left  leg) 


J4  Graphic  Aids  to  Diagnosis 

lead  I 
Current  from  right  arm  and  left  arm. 

LEAD  II 

Current  from  right  arm  and  left  leg. 

LEAD   III 

Current    from  left   arm   and  left  leg. 

Electrocardiograms  obtained  from  a  normal  individual  by  the 
three  leads  as  described  present  different  features.  The  wave 
i/'i  is  positive  in  all  leads.  (P)  to  (R)  interval  varies  slightly 
in  the  three  leads.  All  the  waves  of  lead  n  are  greater  than  those 
of  leads  i  and  [II.  The  wave  ( 1\ )  is  positive  in  all  leads.  (T)  is 
usually  positive  in  all  leads,  but  is  occasionally  negative  in  lead  III. 
Even  in  normal  individuals  there  is  a  considerable  range  of  variation 
in  the  electrocardiogram  which  lies  within  the  limits  of  the  normal. 
Among  these  physiological  variations  may  be  mentioned  a  shorten- 
ing of  the  diastolic  period  in  increased  frequency  of  the  heart,  and 
variation  in  the  aptitude  of  the  (R)  wave  synchronous  with  respira- 
tion;  the  increase  in  the  size  of  the  (T)  wave  with  increased  exer- 
tion; the  changes  in  (Q)  and  (S)  coincident  with  the  changes  of 
the  position  of  the  heart  in  the  thoracic  cavity. 

In  comparing  the  value  of  the  polygram  and  the  electrocardio- 
gram as  means  of  interpreting  the  changes  in  anatomical  and  func- 
tional conditions  of  the  heart  we  should  observe  first  of  all  that 
these  two  methods  record  different  sets  of  phenomena.  The  poly- 
gram is  a  graphic  time  pressure  curve.  The  electrocardiogram  is  a 
graphic  portrayal  of  the  variation  of  electrical  potential  during 
muscular  activity.  By  both  of  these  methods  we  can  study  the 
functions  of  stimulus  production,  irritability,  conductivity  and  con- 
tractility, but  each  method  has  certain  advantages  and  is  successful 
in  points  where  the  other  is  inadequate.  They  do  not  portray  the 
same  phenomena  and  are  therefore  supplemental  and  corroborative 
rather  than  identical.  For  this  reason  we  have  adopted  a  scheme 
for  taking  combined  records,  i.e.,  we  often  record  on  the  same  film 
figures  of  the  electrocardiographic  and  time  pressure  curves  of  the 
arterial  and  venous  pulses.  Conclusions  drawn  from  both  types  of 
records  are  remarkably  in  accord,  thus  strengthening  the  evidence 
obtained. 


Graphic  Aids  to  Diagnosis 


25 


Figure  6 

Diagram  of  the  pressure  changes  in  the  cardiac 
chambers  and  their  time  relations  to  the  aortic, 
carotid,  iugular  and  electrocardiographic  curves 
and  heart   sounds.      (After  Lewis.) 


CHAPTER  V 
Classification  of  Disturbances  of  Myocardial  Function 

The  ideal  analysis  of  myocardial  functions  is  based  on  an  ex- 
amination of  the  fundamental  properties  of  the  muscle  cells.  Such 
an  examination  would  show  that — 

Stimulus  production   is   normal,    increased   or   diminished. 

Excitability       "  "        "  " 

Conductivity      " 

Contractility      " 

Tonicity 

If  there  is  a  departure  from  the  normal  (i.e.,  a  depression  or  an 
increase  in  one  of  these  properties)  the  abnormality  may  involve 
the  entire  musculature  or  a  limited  portion  of  it.  Such  a  classi- 
fication should  therefore  indicate  the  location  or  site  of  the  ab- 
normality. That  is  to  say,  it  should  indicate  the  particular  part  in- 
volved, as,  for  example,  the  sinus  node,  the  auricular  tissue,  the 
auriculoventricular  node,  the  bundle  of  His  or  one  of  its  branches,  the 
ventricular  muscle,  etc.,  etc. 

To  complete  such  a  classification  the  etiological  condition  should  he 
investigated  and  we  should  assign  the  change  in  function  to  some 
underlying  condition,  anatomical,  nutritional,  reflex,  etc. 

While  at  present  the  state  of  our  knowledge  and  our  means  of  ob- 
taining evidence  in  regard  to  all  these  factors  are  too  incomplete  to 
permit  us  to  make  a  final  analysis  in  every  instance  and  to  assign 
the  existing  abnormality  to  a  definite  change  in  one  or  more  of 
the  fundamental  properties  of  cardiac  muscle,  with  an  exact  site 
and  an  accurate  causal  factor,  we  are  able  to  accomplish  this  to  a 
limited  extent,  but  the  advances  of  the  past  decade,  the  result  of 
careful  clinical  observations  and  well-conceived  experiments  on 
animals  give  us  promise  of  a  more  extensive  knowledge  in  the  near 
future.  It  is  important  that  the  study  of  remedies  should  be  based 
upon  a  similar  analysis  so  that  we  may  know,  for  example,  whether 
a  particular  drug  or  hydrotherapeutic  procedure  will  heighten  or 
depress  excitability  in  a  particular  portion  of  the  heart  and  thus  lead 

26 


Disturbances  of  Myocardial  Function  27 

us  to  its  logical  utilization  in  correcting  an  abnormal  state  of  this 
property. 

As  an  example  of  the  present  possibilities  of  the  use  of  such 
a  classification,  we  may  cite  a  case  in  which  we  have  evidence  that 
all  the  fundamental  properties  arc  normal  except  that  of  conduction. 
We  may  also  have  evidence  that  the  conduction  is  depressed  and 
that  the  abnormality  is  localized  in  the  cells  of  the  bundle  of  1  lis,  if 
the  patient  has  been  taking  large  doses  of  digitalis  (we  know  that 
digitalis  depresses  conductivity),  we  may  find  that  the  withdrawal 
of  this  drug  allows  the  cells  to  recover  their  property  of  conduc- 
tion to  the  normal  degree. 

CLINICAL    CONSIDERATIONS 

For  the  clinician  one  of  the  most  common  and  often  an  early 
feature  of  change  in  myocardial  function  is  an  alteration  in  the 
rate  and  rhythm  of  the  heart  action.  Since  we  are  to  consider  these 
myocardial  changes  from  the  standpoint  of  the  everyday  practitioner 
it  will  be  well  for  us  to  take  our  start  from  this  point,  and  to 
subdivide  our  cases  into  classes,  grouped  on  the  basis  of  easily 
elicited  physical  signs,  viz.  varieties  of  rate  and  rhythm.  By  the 
employment  of  graphic  methods  and  other  means  at  our  disposal  we 
will  endeavor  to  further  analyze  each  group  and  to  point  out  as 
far  as  we  are  able  the  fundamental  properties  which  are  disordered, 
the  site  of  the  abnormality  and  its  cause.  We  will  therefore  con- 
sider our  cases  in  the  following  groups : 

A  Regular. 
B  Irregular. 

1.  Bradycardia. 

2.  Tachycardia. 

3.  Sinus  arrhythmias. 

4.  Extrasystoles. 

5.  Alternation. 

6.  Complete  irregularity. 

THE   REGULAR   HEART 

By  the  term  regular  heart  we  understand  one  which  conforms  to 
the  rule   (regula)  of  the  normal  heart.      As  opposed  to  the  term 


28  Disturbances  of  Myocardial  Function 

regular,  the  term  irregular  heart  includes  nil  changes  in  rate,  rhythm 
and  character  of  cardiac  contractions  which  do  not  conform  to  the 
rule   of   the   normal    heart. 

What  then  are  the  rules  of  the  normal  heart  heat? 

i.  The  rate  of  the  normal  heart  is  not  fixed  at  any  definite 
figure ;  it  is  dependent  on  the  needs  of  the  body  at  any  particular 
moment.  The  heart  is  a  pump  which  has  its  greatest  efficiency  when 
it  is  maintaining  the  needs  of  the  individual  organism  with  the 
least  expenditure  of  cardiac  energy.  Any  very  considerable  varia- 
tion in  rate  will  either  fail  to  meet  the  needs  of  the  body,  or  will 
meet  these  needs  with  lack  of  economy  in  the  expenditure  of  energy. 
Hence,  the  rate,  whether  too  fast  or  too  slow,  which  per  se  falls 
short  in  maintaining  an  adequate  circulation  or  which  does  this 
with  an  undue  expenditure  of  energy,  is  inefficient  and,  therefore, 
not  according  to  the  rule  of  the  normal  heart. 

Within  such  limits  the  rate  may  vary  and  yet  be  normal,  but 
such  variations  must  be  gradual.  Change  in  rate  in  the  normal 
heart  is  accomplished  by  a  change  in  the  length  of  the  diastolic 
period,  but  to  conform  to  the  rule  the  difference  in  length  of  suc- 
cessive diastolic  periods  must  be  infinitesimal.  A  regular  heart  always 
has  a  rate  within  the  normal  limits,  but  a  heart  with  a  normal  rate 
may  be  irregular  since  in  some  other  features  it  does  not  conform  to 
the  rule  of  the  normal  heart, 

2.  The  rhythm;  the  rule  of  the  normal  heart  is  that  it 
must  not  only  beat  rhythmically,  but  also  that  the  rhythm  must 
have  a  special  well-defined  character ;  the  individual  cycles  which 
compose  the  rhythm  must  all  be  of  the  same  kind  and  size,  and 
the  diastolic  portions  of  successive  cycles  must  be  of  equal  length. 

A  regular  heart  is  always  rhythmic,  but  a  rhythmic  heart  is  not 
necessarily  regular. 

The  pulsus  altcrnans  is  an  example  of  heart  activity  which 
is  perfectly  rhythmic  and  yet,  according  to  our  definition,  is 
irregular;  it  is  composed  of  alternating  large  and  small  beats  which 
succeed  each  other  at  equal  intervals  and  is  therefore  absolutely 
rhythmic,  yet  since  the  kind  of  rhythm  does  not  conform  to  the 
rule,  since  successive  beats  are  unequal  in  size,  it  falls  into  the 
class  of  irregularities. 

3.  The    pacemaker    of    the    regular    heart    is    the    sinus    node; 


Disturbances  of  Myocardial  Function  29 

when  any  other  portion  of  the  heart  cither  customarily  or  occasion- 
ally initiates  the  stimulus  which  results  in  a  contraction,  this  heart 
must  be  included  in  the  class  of  irregular  hearts. 

4.  In  the  regular  heart  the  wave  of  contraction  must  sweep  over 
its  chambers  in  an  orderly  sequence  and  the  stimulus  must  follow 
the  path  which  zve  have  learned  to  recognize  as  normal.  Any  devia- 
tion in  the  path  which  the  stimuli  follows  or  any  abnormality  in  the 
sequence  of  contraction  of  the  chambers  brings  it  into  the  group  of 
irregular  hearts. 

5.  In  the  regular  heart  not  only  must  the  stimulus  sweep  over 
the  heart  by  the  normal  paths  and  in  the  normal  direction,  but  it 
must  travel  at  a  speed  which  is  normal.  Any  delay  in  transmitting 
stimuli  places  a  heart  among  those  classified  as  irregular. 

6.  Among  other  features  to  which  the  heart  must  conform  to  be 
considered  regular  are  uniformity  in  the  size  and  duration  of  suc- 
cessive systoles,  and  a  condition  of  the  muscle  mass  which  is  some- 
what short  of  complete  relaxation  during  diastole. 

The  departure  from  the  normal  in  (1)  rate  and  (2)  rhythm 
are  easily  detected  by  the  ordinary  methods  of  inspection,  palpation 
and  auscultation.  An  abnormal  (3)  pacemaker;  an  unusual  (4) 
path  or  direction  taken  by  the  stimulus;  (5)  a  delay  in  the  speed 
of  the  passage  of  the  stimulus  and  the  finer  variations  (6)  in  the 
character  of  the  contractions  of  the  ventricles  are  often  best  de- 
tected by  the  employment  of  graphic  methods,  but  when  one  has 
once  become  familiar  with  the  evidence  obtained  by  such  means, 
physical  signs  are  quite  sufficient  in  the  majority  of  instances  to 
afford  us  data  upon  which  to  base  a  correct  interpretation  of  the 
abnormalities  which  are  present. 

THE  IRREGULAR  HEART 

In  the  preceding  section  it  was  stated  that  the  group  of  irregular 
hearts  includes  all  those  which  show  a  departure  from  the  normal 
in  rate,  rhythm  and  character  of  contractions.  In  the  succeeding 
paragraphs  an  attempt  was  made  to  define  the  "rules"  of  normal 
cardiac  activity.  We  will  next  consider  the  various  types  of  irregular 
hearts  which  are  distinguished  by  well-defined  changes  in  rate  and 
rhythm. 


30  Disturbances  of  Myocardial  Function 

ABNORMAL   CHANGES   IN   RATE 

Under  irregularities  of  the  heart  are  included  all  those  changes 
of  rate  which  exist  at  the  expense  of  the  functional  efficiency  of  the 
heart.  The  normal  heart  is  a  machine  which  provides  the  individual 
at  any  particular  moment  with  a  sufficient  hlood  supply,  and  at  the 
same  time  is  working  with  an  economical  expenditure  of  energy; 
it  is  working  at  an  optimum.  The  adaptation  of  the  rate  of  the 
heart  to  the  needs  of  the  body  is  controlled  very  largely  through  the 
extracardial  nerves.  Anatomical  and  functional  evidences  show  that 
for  the  most  part  the  fibers  of  the  right  vagus  and  the  right  accele- 
rator (sympathetic)  nerves  terminate  in  the  tissues  in  the  region  of 
the  sinus  node  while  the  left  vagus  and  left  accelerator  are  more 
particularly  distributed  to  the  auriculo-ventricular  node  and  the  tis- 
sues junctional  between  the  auricle  and  ventricle.  By  reflex  activity 
through  these  paths  the  rapidity  of  stimulus  production  is  modified. 
There  is  considerable  physiological  and  clinical  evidence  that  both 
these  nerves  possess  what  is  known  as  "tone,"  that  their  activity  is 
continuously  modifying  the  stimulus  production  of  the  cells  of  the 
heart ;  the  vagus  tends  to  hold  this  property  in  check,  the  accelerator 
tends  to  heighten  its  activity ;  it  is  through  a  correct  balance  of  these 
forces  that  the  heart  activity  is  varied  with  the  momentary  demands 
of  the  organism. 

Hypertonus  of  either  of  these  nerves  results  in  a  heart  rate  ab- 
normally rapid  or  abnormally  slow. 

Among  the  factors  which  modify  the  rate  of  the  heart  are  indi- 
vidual differences  in  the  age,  size  of  body,  build,  work,  temperature, 
nervous  constitution,  arterial  pressure,  etc.,  etc. 


CHAPTER  VI 
Bradycardia.     Heart  Block 

It  is  well  to  recall  first  of  all  that  a  slow  pulse  is  not  necessarily 
synonymous  with  a  slow  heart.  The  heart  contractions  may  be  of 
such  unequal  strength  that  only  a  portion  of  them  are  detected  in 
the  radial  artery;  some  of  the  systoles  may  be  so  lacking  in  force 
that  the  resulting  arterial  wave  may  be  insufficient  to  affect  the 
pressure  in  the  radial  artery,  or  again  they  may  even  fail  to  open  the 
aortic  valves  (pulsus  frustrans).  We  should  therefore  always  check 
up  our  finding  of  a  slow  pulse  by  counting  the  apex  beat  by  ausculta- 
tion. Hence  a  radial  count  alone  is  not  sufficient  to  establish  the 
existence  of  a  bradycardia. 

All  really  slow  hearts  are  comprised  in  two  classes : 

1.  True  Bradycardia. 

2.  Heart  Block. 

i.  In  true  bradycardia  all  the  chambers  of  the  heart  contract 
at  a  slow  rate  and  in  the  normal  sequence  and  relationship. 
It  might  be  fairly  questioned  whether  such  hearts  should  be  in- 
cluded in  the  class  of  irregular  hearts,  since  although  slow,  their  ac- 
tivity is  usually  efficient  in  maintaining  an  adequate  circulation, 
economical  in  the  expenditure  of  energy,  and  in  other  respects  con~ 
forming  to  the  rules  of  the  normal  heart.  However,  some  of  these 
hearts  are  too  slow  to  properly  supply  all  parts  of  the  organism  with 
sufficient  blood,  and  therefore  this  group  of  bradycardias  may  fairly 
be  included  among  the  irregular  hearts. 

A  slow  heart  is  not  a  very  rare  occurrence,  a  rate  between  50  and 
60  is  common  in  tall  persons,  in  those  with  increased  arterial  pres- 
sure, aortic  stenosis,  pregnancy,  convalescence  from  acute  fevers,  in 
typhoid  fever,  meningitis,  chronic  nephritis,  cerebral  hemorrhage 
and  tumors;  it  is  often  associated  with  jaundice  and  some  digestive 
reflexes,  such  as  vomiting,  etc.  When  we  attempt  to  classify  these 
heterogeneous  clinical  manifestations  it  seems  reasonable  to  divide 
them  into  two  groups : 

3i 


3-j  Bradycardia.     Heart  Block 

i  a  I  Toxic  agents,  which  probably  have  a  direct  depressing  ef- 
fect on  the  sinus  node   (typhoid   fever,  jaundice). 

( /> )  Heightened  vagus  tone,  cither  from  direct  irritation  of  the 
pneumogastric  center  (meningitis,  cerebral  hemorrhage),  or  a  reflex 

activity    (vomiting,  pregnancy,   increased  arterial   tension,   etc.). 

It  is  to  be  noted  that  a  true  bradycardia  is  due  to  a  depression 
of  activity  of  the  sinus  node,  either  through  the  chemical  constitution 
of  its  blood  supply,  or  through  the  nervous  influences  brought  to  it 
through  the  extracardial  nerves,  particularly  the  right  vagus.  The 
change  which  takes  place  in  the  node  is  a  depression  of  the  property 
of  the  formation  of  stimulus  material  or  of  its  excitability,  or  both; 
at  present  we  have  no  clinical  method  of  determining  which  one  of 
these  properties  is  the  one  affected  in  any  particular  case. 

At  a  later  time  the  effects  of  vagus  activity  will  be  more  fully 
discussed  ;  in  passing  it  will  be  sufficient  to  note  that  by  the  adminis- 
tration of  atropin,  vagus  impulses  may  be  cut  off  and  thus  a  clinical 
estimate  may  be  made  of  the  influence  which  it  has  hitherto  been 
exerting. 

A  true  bradycardia  is  never  encountered  with  a  rate  under  40. 
Probably  every  heart  with  a  rate  less  than  this  belongs  to  the  second 
group  of  slow  hearts,  viz. : 

HEART  DLOCK 

2.  Which  is  the  result  of  interference  in  the  conduction 
of  stimuli  from  one  part  of  the  heart  to  another.  Theoretically 
such  an  abnormal  condition  may  occur  in  any  part  of  the  mus- 
culature of  the  heart;  practically  it  is  rarely  recognized,  except 
when  it  involves  the  bundle  of  His  or  one  of  its  branches.  Here 
the  cells  of  the  conducting  system  are  grouped  in  a  narrow  band 
so  that  a  very  limited  lesion  or  functional  derangement  of  moderate 
extent  is  sufficient  to  produce  marked  clinical  phenomena. 

In  accordance  with  the  degree  of  functional  disorder  we  may 
recognize : 

(a)  Total  Heart  Block,  complete  dissociation. 

(b)  Partial  Heart  Block,  partial  dissociation. 

(c)  Delayed  Conduction,  without  dissociation. 


Bradycardia.     Heart  Block  33 

ytt)  TOTAL  HEART  BLO<  K  ;  COMPLETE  DISSOCIATION 

It  will  be  recalled,  as  was  pointed  out  in  the  paragraphs  on  the 
anatomy  and  function  of  the  heart  tissue,  that  stimuli  normally 
originate  in  the  sinus  node,  thence  spread  over  the  auricle  to  the 
auriculo-ventricular  node  of  Tawara,  where  connection  is  made  with 
the  bundle  of  His;  through  this  the  impulses  pass  to  be  distributed 
first  by  the  two  branches  of  the  bundle,  and  later  by  its  subdivisions 
and  their  connections  with  the  Furkinjc's  fibers  to  all  parts  of  the 
ventricular  muscle.  It  will  also  be  recalled  that  in  the  Stannius  ex- 
periment on  the  frog's  heart,  when  the  second  cut  or  ligature  is 
applied  so  as  to  separate  the  auricle  and  the  ventricle,  the  auricle 
continues  to  contract  rhythmically  in  the  normal  manner  and  after 
a  considerable  pause  the  ventricle  begins  to  contract  at  a  slow 
rhythm  entirely  independent  of  the  auricular  contractions.  This  is 
precisely  what  happens  in  man  when  the  property  of  conduction  of 
the  bundle  of  His  is  destroyed.  The  auricles  continue  to  contract  in 
a  normal  manner  in  response  to  the  rhythmic  stimuli  arising  in  the 
sinus  node ;  these  impulses  are  unable,  however,  to  pass  the  obstruc- 
tion in  the  bundle  of  His  and  hence  are  unable  to  influence  the  ac- 
tivity of  the  ventricle.  Since,  however,  the  uninjured  portions  of 
the  bundle  still  possess  the  fundamental  properties  of  the  production 
of  stimulus  material  and  excitability,  stimuli  will  be  set  free  at  this 
point  and  the  ventricle  will  respond  by  slow  rhythmic  contractions 
entirely  independent  of  the  contractions  of  the  auricle  and  of  the 
stimuli  originating  in  the  normal  pacemaker.  This  condition  is 
known  as  complete  dissociation  and  the  activity  of  the  ventricle  as 
the  ideo-ventricular  rhythm. 

(b)    PARTIAL   HEART  BLOCK  J   PARTIAL  DISSOCIATION 

If  the  bundle  of  His  is  not  completely  functionally  severed  but  is 
merely  injured  so  that  the  property  of  conduction  is  depressed  (that 
is  to  say  if  the  formation  of  the  molecules  upon  which  the  con- 
duction of  impulses  is  dependent  is  abnormally  slow)  the  ventricle 
may  not  respond  to  every  impulse  from  the  auricle.  This  condition 
is  known  as  partial  dissociation.  If  the  ventricle  ordinarily  responds 
to  the  stimuli  from  the  normal  pacemaker,  and  only  occasionally 
fails  to   contract   in   this   manner,   the  condition   is  known  as  the 


34  Bradycardia.     Heart  Block 

dropped  beat.  If  the  ventricle  responds  to  every  second  or  third 
auricular  contraction  it  is  called  a  2  to  i  or  a  3  to  1  rhythm.  Or, 
if  for  every  5  beats  of  the  auricle  we  have  3  contractions  of  the 
ventricle  the  condition  is  known  as  partial  dissociation  with  a  ?  to  5 
rhythm.  At  times  the  periods  of  ventricular  response  may  he  so 
long  that  an  occasional  stimulus  may  be  initiated  in  the  bundle  and 
we  then  have  a  partial  dissociation  with  interspersed  ideo-voitricular 
contractions  {"escape  of  the  ventricle"). 

(C)   DELAYED  CONDUCTION    WITHOUT  DISSOCIATION 

The  conducting  tissues  may  be  so  affected  that  the  rate  of  con- 
duction may  be  much  less  than  the  normal  so  that  the  passage  of 
the  stimulus  from  the  auricle  to  the  ventricle  consumes  a  period  of 
time  appreciably  in  excess  of  what  is  usual;  if,  however,  the  ven- 
tricle responds  to  each  stimulus  originating  at  the  pacemaker  there 
is  no  dissociation.  This  form  of  impaired  function  may  easily  pass 
over  to  a  partial  heart  block,  or  even  a  complete  block  and  a  single 
case  may  exhibit  grades  of  conduction  changes  comprising  delayed 
conduction,  partial  and  complete  block  on  successive  observations. 

TATIIOLOGY 

Heart  block  of  all  degrees  has  been  produced  experimentally 
by  various  procedures  which  have  had  for  their  object  the 
destruction  or  injury  of  the  bundle  of  His.  Ligature  of  the 
bundle  in  the  perfused  heart  (Humblet)  and  the  dog's  heart  in  situ 
(Erlanger),  crushing  by  means  of  an  auriculo-ventricular  clamp 
(Erlanger),  section  of  the  bundle  in  the  perfused  heart  (Cohn  and 
Trendelenburg)  have  uniformly  produced  some  degree  of  block 
whenever  subsequent  histological  examination  demonstrated  injury 
to  the  bundle.  Heart  block  has  been  produced  by  stimulation  of  the 
vagus  (Chauveau)  and  as  a  direct  result  of  asphyxia  (Lewis,  Sher- 
rington). Various  degrees  of  temporary  or  permanent  block  have 
been  produced  by  the  injection  of  various  cardiac  poisons  such  as 
digitalis  (Cushny,  Tabora),  adrenalin  (Kahn),  aconite  (Cushny), 
muscarine  and  physostigmine  (Rothberger  and  W'interberg). 

Cases  which  have  exhibited  the  evidence  of  heart  block  have 
almost  invariably  shown  some  histological  alteration  in  the  bundle 


Bradycardia.     EJeart  Block 

of  His  when  such  an  examination  has  been  made.  As  a  gen- 
eral rule  the  degree  of  heart  block  corresponds  with  the  extent  of  the 
histological  change  which  is  found  in  the  bundle;  a  complete  heart 
block  usually  corresponds  to  a  complete  destruction  of  the  bundle, 
while  delayed  conduction  is  more  apt  to  be  associated  with  a 
moderate  degree  of  infiltration,*  in  the  exceptional  case  a  complete 
block  may  occur  with  but  very  little  apparent  histological  changef 
and  a  case  of  partial  block  may  exhibit  an  extreme  degree  of 
bundle  destruction.  These  exceptional  cases  merely  emphasize  the 
fact  that  histological  observations  cannot  always  be  relied  on 
to  measure  the  degree  of  functional  impairment. 

Bachmann$  has  collected  from  the  literature  sixty-three  cases 
of  heart  block  reported  since  1899.  Complete  clinical  and  histolog- 
ical data  wrerc  obtained  in  twenty-four  or  these ;  in  the  others  the 
information  obtained  was  interesting,  but  incomplete  in  all  details. 
In  all  cases  where  a  complete  transverse  lesion  was  found,  there 
had  been  a  complete  heart  block.  In  a  group  of  cases  showing  varia- 
tions from  partial  to  complete  block,  the  extent  of  the  histological 
examination  did  not  show  changes  which  could  be  regarded  as  pro- 
portional to  the  degree  of  functional  disturbance.  In  five  cases, 
including  those  showing  both  partial  and  complete  block,  no  histo- 
logical alterations  in  the  bundle  of  His  were  found.  Bachmann 
calls  attention  to  the  fact  that  other  parts  of  the  conducting  system 
were  not  minutely  studied,  hence  the  evidence  of  absence  of  all 
histological  change  is  not  absolutely  conclusive  in  these  cases. 

Probably  the  lesion  of  the  bundle  of  His  wdiich  has  been  most 
frequently  found  is  the  result  of  a  syphilitic  infection,  either  a 
gumma  or  an  old  syphilitic  scar.  Calcareous  nodules,  chronic  inflam- 
matory changes,  fibrosis,  calcareous  degeneration  and  necrosis  in- 
volving the  bundle,  have  been  found ;  more  rarely  an  ulcer 
penetrating  the  septum ;  atheromatous  changes  in  the  central  fibrous 
body ;  fibroid  and  epithelial  tumors  have  been  described.  Acute 
inflammatory  conditions  may  be  present  with  leukocyte  infiltration 
and  degeneration  of  the  cells  of  the  bundle. 

*Pardee:  Arch.  Int.  Med.,  1913,  xi,  641. 
fKrumbhaar :  Arch.  Int.  Med.,  1910,  v,  583. 
^Bachmann :  Jour.  Exp.  Med.,  1912,  xvi,  25. 


36  Bradycardia,     Heart  Block 

etiology 

In  addition  to  the  cases  of  distinct  syphilitic  origin,  others 
Seem  to  hear  a  direct  relationship  to  the  more  acute  infections. 
More  or  less  severe  cases  of  heart  block  have  followed  diph- 
theria, typhoid  fever,  influenza,  septic  poisoning,  puerperal  fever 
and  pneumonia  ;  these  diseases  naturally  supply  the  etiological  factor 
in  heart  block  as  found  in  youth  and  young  adults.  In  elderly 
people  the  lesion,  when  not  syphilitic,  is  often  merely  a  phase  of 
one  of  the  common  general  chronic  inflammatory  or  degenerative 
processes,  whose  etiology  is  still  for  the  most  part  shrouded  in  so 
much  obscurity.  The  degenerative  changes  accompanying  arterio- 
sclerosis of  the  coronary  arteries  are  sometimes  associated  with 
various  degrees  of  heart  block. 

There  is  a  group  of  cases,  the  majority  of  which  show  only 
mild  grades  of  interference  with  conduction,  which  are  undoubtedly 
of  rheumatic  origin.  Mackenzie  was  the  first  to  draw  attention  to 
this  group.  Many  of  them  have  had  pericarditis  or  endocarditis 
particularly  with  involvement  of  the  mitral  valve.  There  seems 
to  be  little  question  that  the  acute  and  subacute  rheumatic  inflam- 
matory processes  have  a  tendency  to  implicate  not  only  the  peri- 
cardium and  the  endocardium,  but  the  myocardium  as  well.  Keith's 
examination  of  hearts  which  had  been  observed  clinically  by  Mac- 
kenzie* showed  that  the  inflammatory  process  had  a  tendency 
''to  extend  from  the  base  of  the  valve  into  the  central  fibrous 
body,  and  to  involve  the  bundle." 

It  has  been  pointed  out  that  experimentally  toxic  doses  of  digi- 
talis may  produce  block  in  the  normal  heart ;  the  administration 
of  such  doses  is,  of  course,  impossible  in  many,  but  the  effect  of 
moderate  doses  of  digitalis  and  other  drugs  of  the  same  group 
on  hearts  with  impaired  conduction  may  often  be  observed  in  the 
clinic.  Given  in  such  cases  digitalis  usually  lengthens  the  con- 
duction time  and  may  even  induce  a  partial  or  a  complete  block. 
The  question  is  still  unsettled  as  to  whether  digitalis  acts  in  these 
cases  directly  on  the  heart  tissues  or  through  the  vagus  nerve. 

Heart  block  has  been  produced  experimentally  by  stimulation  of 
the  vagus  nerve.     It  is  a  question  whether  a  clinical  heart  block 

♦Mackenzie:   Diseases  of   the    Heart,   p.    179. 


Bradycardia.     1 1  eari    Blo<  k 


37 


As 
A-V 


V. 


Figure  7 
delayed   conduction  producing  partial  block 


Aj 

A-V 

V5 


1   1 

1 

1      1 

\               \                \                                   \- 

Figure  8 
partial  block 


A-V 
Vs 


Figure  9 
complete  block 


Diagrams  showing  the  mechanism  of  various  degrees  of  heart  hlock.  As  =  auric- 
ular contraction.  A-V  =  conduction  from  auricle  to  ventricle  (note  the  variation 
in  the  length  of  this  period).     Vs  =:  ventricular  contractions. 


38  Bradycardia.     Heart  Block 

can  be  initiated  by  vagal  changes,  but  in  damaged  hearts  the  con- 
duction abnormalities  may  be  accentuated  by  vagal  reflexes.  A 
very  beautiful  illustration  of  this  influence  is  a  case  reported  by 
Mackenzie*;  the  conduction  time  was  usually  slow  and  the  reflex 
obtained  by  swallowing  repeatedly  produced  a  partial  block  when 
the  patient  was  under  the  influence  of  digitalis.  Conduction  dis- 
turbances following  vagus  stimulation  have  been  studied  by  Robin- 
son and  Draper, f  who  have  published  some  very  beautiful  electro- 
cardiograms showing  changes  in  conduction  of  various  degrees. 
They  reached  the  conclusion  that  the  left  vagus  has  as  a  rule  a 
greater  influence  on  the  property  of  conduction  than  the  right 
vagus. 

IDENTIFICATION 

Clinical:  When  the  pulse  rate  is  under  60  one  may  sus- 
pect some  degree  of  interference  with  the  property  of  conduc- 
tion ;  in  such  a  case,  however,  one  should  always  compare  the 
rate  of  cardiac  contractions  as  determined  by  auscultation  with  the 
pulse  rate,  since  not  infrequently  one  finds  a  large  number  of 
ventricular  systoles  which  are  so  inefficient  as  to  make  no  im- 
pression on  the  radial  pulse  (when  at  a  later  time  wc  take  up  the 
discussion  of  extrasystoles  and  auricular  fibrillation  it  will  be 
pointed  out  that  in  these  conditions  many  ventricular  contractions 
may  be  detected  on  auscultation  over  the  precordium  which  afford 
in  the  radial  artery  no  evidence  of  their  presence). 

If  the  heart  is  perfectly  rhythmic  and  has  a  rate  in  the  neigh- 
borhood of  30  it  is  practically  certain  that  a  complete  block  is 
present.  A  faster  ventricular  rate  does  not,  however,  rule  out 
the  possibility  of  a  complete  block,  8  out  of  34  cases  of  complete 
block  which  I  have  studied  by  graphic  methods  had  a  ventricular 
rate  of  over  45. 

In  a  partial  block  the  ventricle  may  contract  rhythmically  or  at 
times  may  be  quite  arrhythmic,  the  rate,  while  usually  a  slow 
one,  is  as  a  rule  faster  than  in  complete  block.  A  partial  block 
is  to  be  suspected  when  the  ventricular  rate  suddenly  changes 
to  one  half  its  former  rate.     A  single  dropped  beat  is  usually  due 

*Ibid.,  p.  340,  also  Plate  IV,  Figs.  258  and  259. 
tjour.  of  Exper.  Med.,  xv,  No.  I,  1912. 


Bradycardia.    Heart  Block 


3'J 


;■  .''..' 


Brachial 


0.2  second 


Figure  io 

Delayed   conduction.      No  dissociation,      a-c   interval    =    0.3   second.      Auricular    rate    =    73- 
Ventricular  rate   =   73. 


Jugular 


Erachial 


0.2  second 


Figure  ii 

Partial  block.     For  the  most  part  this  is  a  2  to  1  block,  but  occasionally  an  extra 
auricular  impulse  passes  the  block.    Auricular  rate  =  92.     Ventricular  rate  —  42. 


Jugular 


Brachial 


0.2  second 


Figure  12 

Complete  block.     Auricular  rate  =  9S.     Ideo-ventricular  rate  =  31. 


40  Bradycardia.     Heart  Block 

to  a   partial   block,  but  this  can   only   surely   be   determined   by   the 

evidence  of  graphic  records. 

When  the  pulsations  of  the  jugular  vein  are  visible  they  are 
of  considerable  aid   in   making  a    diagnosis  of   the  character  of    the 

irregularity.  In  complete  block  the  jugular  pulsations  are  usually 
rhythmic,  but  occur  at  much  more  frequent  intervals  than  and 
quite  independent  of  the  ventricular  impulses.  Occasionally  there 
may  be  seen  a  large  jugular  pulsation  in  place  of  one  of  the 
usual  smaller  ones,  and  if  this  phenomenon  is  closely  observed  it 
will  be  apparent  that  it  occurs  at  a  time  when  the  ventricle  con- 
tracts synchronously  with  the  jugular  pulsation,  that  is  when  the 
auricles  and  ventricles  contract  simultaneously.  In  incomplete  block 
the  jugular  pulsations  usually  bear  a  definite  numerical  ratio  to  the 
ventricular  contractions,  for  example,  we  may  see  in  a  2  to  I 
block,  two  jugular  pulsations  to  one  apex  beat,  or  three  jugular  to 
two  ventricular  in  a  3  to  2  block,  etc. 

In  delayed  conduction  it  is  sometimes  possible  to  detect  a  longer 
than  the  normal  interval  between  the  first  venous  wave  and  the 
carotid  pulsation,  or  this  prolonged  interval  may  become  evident 
when  we  note  the  time  by  which  the  first  wave  of  the  jugular 
pulse  precedes  the  apex  beat. 

In  a  few  cases  of  block  a  low  muffled  sound  may  be  heard 
during  ventricular  diastole;  this  is  the  auscultatory  evidence  of  the 
auricular  contraction  which  is  sometimes  heard  ;  when  this  occurs 
soon  after  the  second  sound  or  a  distinct  interval  before  the  first 
sound  it  sometimes  gives  the  impression  of  a  reduplication  of  the 
second  or  of  the  first  sound,  as  the  case  may  be. 

In  certain  cases  of  mitral  stenosis  associated  with  heart  block 
there  have  been  described  (Mackenzie)  short,  harsh  murmurs  which 
occurred  synchronously  with  the  pulsations  of  the  jugular  vein  and 
quite  independent  of  the  ventricular  contractions.  These  were  as- 
cribed to  the  acceleration  of  the  flow  of  blood  from  auricle  to 
ventricle  at  the  time  of  the  independent  auricular  systole.  When 
present  this  sign  should  be  of  assistance  in  recognizing  the  inde- 
pendent activities  of  the  auricles  and  ventricles ;  personally  it  has 
been  my   fortune  to  see  only  one  case  of  this  kind. 

The  Adams-Stokes  syndrome,  attacks  of  unconsciousness  asso- 
ciated with  a  slow  pulse,  should  always  suggest  the  possibility  of 


BR^DVCAKDIA.        llhART     liLOCK 


4' 


Tuff  u  la  r 


Brachial 


Figure  13 

Delayed   conduction       a-c   interval  =  0.35   second. 


A]  • 


Brachial 


Figure  14 

Delayed  conduction.     Apex  and   radial   tracings.      The   auricular   wave   is  seen   in  the 
apex  curve  and  precedes  the  ventricular  wave  by  0.35  second. 


4-j  Bradycardia.     Heart  Block 

heart  block.  It  should  be  remembered,  however,  that  heart  block 
and  the  Adams-Stokes  syndrome  are  not  interchangeable  terms. 

A  fluroscopic  examination  often  will  demonstrate  the  independ- 
ent activities  of  the  chambers. 

Polygraphic  tracings  |  Kigures  10,  n  and  u)  will  usually  give 
conclusive  evidence  of  conduction  defects  when  these  air  present. 
If  this  property  is  only  moderately  depressed,  the  ventricle  (as 
shown  by  the  apex  or  arterial  tracing)  will  have  a  normal  or 
slow  rate  and  the  intersystolic  periods  will  be  uniform  in  length 
(Figure  io),  the  jugular  tracing,  representing  the  activity  of  the 
right  auricle,  will  show  an  a  wave  preceding  each  c  wave  at  a  uniform 
interval,  but  this  a-c  interval  will  exceed  0.2  second,  the  time  occu- 
pied by  the  normal  a-c  interval. 

If  conduction  is  a  degree  more  defective  the  arterial  pulse  may 
show  a  rhythmic  activity  indicated  in  the  diagram  (Figure  7),  the 
diastolic  periods  gradually  increase  in  length  until  the  longest  pause 
is  reached  at  the  time  of  a  "dropped  beat,"  then  suddenly  this 
period  is  shortened  only  to  be  again  gradually  lengthened  until 
another  beat  is  dropped.  When  we  examine  the  auricular  diagram 
wc  see  that  the  auricular  (a)  waves  recur  at  regular  intervals; 
the  a-c  interval  following  the  "dropped  beat"  may  be  normal, 
0.2  second,  in  length (  it  usually  exceeds  this),  but  each  successive 
a-c  interval  is  longer,  since  the  property  of  conduction  is  becoming 
more  and  more  exhausted,  and  each  ventricular  response  is  thus 
delayed  until  one  of  the  auricular  impulses  reaches  the  junctional 
tissues  while  they  are  still  in  the  refractory  state,  hence  no  im- 
pulse is  conveyed  to  the  ventricle  and  a  "dropped  beat"  results. 
At  the  time  of  the  next  auricular  impulse  the  long  preceding  rest 
has  considerably  restored  the  functional  condition  of  the  auriculo- 
ventricular  bundle,  consequently  the  a-c  interval  is  much  shorter 
and  the  ventricular  response  is  prompt.  This  rhythmic  lengthening 
of  the  ventricular  cycle  superficially  resembles  the  respiratory  sinus 
arrhythmia,  it  can  be  differentiated  from  this  condition  by  observ- 
ing that  in  conduction  defects  (1)  the  rhythmic  change  in  the 
length  of  the  ventricular  cycles  is  not  synchronous  with  the  phases 
of  respiration ;  (2)  the  a  waves  of  the  jugular  tracing  are  separated 
by  equal  intervals;  (3)  the  a-c  intervals  exceed  0.2  second. 

When  the  conduction  is  even  more  abnormal  the  arterial  pulse 


Bradycardia.     Heart  Block 


43 


V 

m 

A 

A. 

X? 

1 

1 

V 

M_MJH 

'*  - 

5^ 

MJ-U4 

i-fyyfi.1/ 

A-CAJL 

Jugular 


Brachial 


0.2  seconfl 


Figure  is 

2  to  i  block.     Auricular  rate  70.     Ventricular  rate  35. 


Jugular 


Brachial 


Figure  16 
Complete  block 


44  Bradycardia,     Heart  Block 

will  be  slow  (usually  40  to  50  per  minute).  In  the  jugular  record 
rhythmically  recurring  a  waves  will  be  found  |  Figures  S  and  11  1. 
but  the  ventricle  responds  only  to  every  other  or  every  third  impulse 
from  the  normal  pacemaker.  The  a-c  interval  when  present  may 
be  of  normal  duration;  it  is  usually  prolonged. 

In  complete  block  |  Figures  <>  and  u  |  the  arterial  pulse  is  slow, 
usually  30-35  per  minute  and  perfectly  rhythmic,  in  the  jugular 
tracing  are  found  the  equally  spaced  a  waves  which  hear  no 
fixed  relation  to  the  ventricular  waves.  The  a  waves  are  equi- 
distant from  one  another  as  are  also  the  c  waves  but  the  two 
rhythms  are  entirely  independent  of  one  another. 

The  Electrocardiogram  furnishes  evidence  of  conduction  defects 
which  is  even  more  clear  than  the  polygram. 

As  has  been  pointed  out,  the  P  wave  represents  auricular  activity, 
0  R  S  T  ventricular  activity.  Normally  the  P-R  interval,  measured 
from  the  beginning  of  the  P  wave  to  the  beginning  of  the  R  wave,  is 
between  0.14  and  0.1S  second;  a  P-R  interval  occupying  more  than 
0.18  second  indicates  a  delay  in  the  passage  of  the  stimulus  from 
the  auricle  to  the  ventricle  and  is  due  to  a  defect  in  t he  property 
of  conduction. 

The  simplest  form  of  this  irregularity  is  shown  in  Figures  17,  -'i 
and  22,  the  pulse  is  beating  slowly  and  rhythmically  at  a  rate  of 
60.  Each  ventricular  complex  is  of  the  normal  type  and  is  pre- 
ceded by  a  P  wave;  the  P-R  interval  is  always  of  the  same  length, 
but  is  excessively  long,  measuring  0.37  second  (Figure  17).  Such 
a  heart,  on  physical  examination,  might  show  little  deviation  from 
the  normal,  but  the  electrocardiogram  makes  very  evident  the  under- 
lying defect. 

The  records  of  cases  of  partial  block  resulting  in  the  "dropped 
beat"  is  shown  in  Figures  18  and  23.  The  P  waves  are  picked  out 
from  such  a  record  with  little  difficulty.  The  ventricular  complexes 
(Q  R  S  T)  are  quite  normal  in  form  except  when  they  are  dis- 
torted by  a  superimposed  P  wave.  The  P  waves  of  the  first  two 
cycles  shown  in  the  record  (Figure  18)  are  easily  recognized,  if  one 
measures  the  time  between  these  P  waves  (approximately  0.6  sec- 
ond )  and,  beginning  with  one  of  these  easily  identified  P  waves,  lays 
off  on  the  remainder  of  the  record  intervals  similar  in  length,  one 
will    find   at   each   one  of   these   points  a   wave  either   clearly  de- 


Figure  17 

Delayed  conduction.  Every  ventricular  complex  (QRST)  is  preceded  by  an  auricular 
complex  (P)-.  The  PR  interval  is  excessively  long,  0.37  second.  The  notch  in  the  P 
wave  is  a  slight  abnormality  not  infrequently  seen  in  cases  of  mitral  stenosis.  Auricular 
rate  —  60.     Ventricular  rate  =  60. 


Figure  18 

Partial  block.  Auricular  rate  =  102.  Ventricular  rate  =  89.  P-R  =  0.18  to  0.43  second.  Note  grad- 
ual lengthening  of  the  P-R  interval  resulting  in  the  "escape  of  the  ventricle  at  x,  also  the  rhythmic  lengthen- 
ing and  shortening  of  the  ventricular  cycles.  P  recurs  at  equal  intervals  of  time,  but  its  relation  to  the 
ventricular  waves  varies,  note  how  the  P  wave  distorts  Q.R.S.  and  T  at  various  points. 


*    1 
s 


Us      t- 


5j 


X 


s 


55 


O.l  '5tean3T" 


Figure  19 

Partial  (2  to  1)  block.  Auricular  rate  =  86.  Ventricular  rate  =  43-  Every  other  auricular  impulse  is 
blocked.  P-R  interval  =0.15  second.  _Note  alternate  short  and  long  auricular  cycles  (sinus  arrhythmia)  and 
slow  regular  contractions  of  the  ventricle. 


Figure  20 

Complete  block.  Auricular  rate  60.  Ventricular  rate  37-  The  auricular  and  ventricular  activities  are 
entirely  independent  of  each  other.  Note  P  is  slightly  notched.  The  ventricular  complex  (RbT)  is  normal 
in  type  except  when  distorted  by  a  superimposed  P  wave. 


4<>  Bradycardia.     Heart  Block 

fined  or  appearing  as  a  notch  changing  the  normal  form  of  the 
ventricular  complex;  these  are  the  P  waves  representing  the 
auricular  activity  which  recur  rhythmically  at  equal  time  intervals. 
The  P-R  intervals  vary  in  length  from  0.18  second  to  0.43  second; 
this  gradually  lengthening  indicates  a  progressive  exhaustion  of 
conductivity,  at  last  (at  x)  the  period  becomes  so  long  that  the 
ventricle  contracts  spontaneously  (known  as  the  "escape  of  the 
ventricle")  without  waiting  for  an  impulse  to  reach  it  from  the 
normal  pacemaker;  the  auricular  impulse  (indicated  by  the 
P  which  merely  notches  the  ascending  limb  of  the  R  wave  at  x) 
reaches  the  ventricle  while  it  is  in  the  refractory  period,  hence  there 
is  no  ventricular  response  to  this  impulse.  After  the  rest  thus 
afforded  to  the  junctional  tissues  the  ventricle  responds  promptly 
to  the  next  auricular  impulse  and  the  P-R  interval  measures  only 
0.18  second  only  again  to  be  gradually  lengthened.  The  record 
shows  an  auricular  rate  of  102,  a  ventricular  rate  of  89.  The 
mechanism  which  underlies  the  gradual  lengthening  and  the  sud- 
den  shortening  of  the  ventricular  cycles  is  quite  evident. 

Another  type  of  partial  block  is  shown  in  Figures  8  and  19.  In 
this  case  the  ventricle  responds  to  every  other  auricular  impulse.  The 
P-R  interval  conforms  to  the  normal  length  (0.15  second)  but  the 
exhaustion  of  the  A-V  bundle  is  shown  in  its  inability  to  transmit 
the  next  succeeding  impulse  coming  down  from  the  sinus,  so  that 
ventricular  responses  and  "dropped  beats"  alternate,  showing  a 
2  to  1  block.  The  existence  of  a  sinus  arrhythmia  evidenced 
by  the  alternating  short  and  long  periods  between  the  auricular 
contractions,  may  be,  in  this  case,  an  additional  element  in  favor- 
ing a  partial  block.  If  the  auricular  responses  were  equidistant 
it  is  quite  possible  that  the  junctional  tissues  would  have  re- 
covered sufficiently  to  convey  the  impulse  to  the  ventricle,  but 
the  shortened  auricular  diastole  which  regularly  follows  a  ven- 
tricular response  does  not  allow  enough  time  for  the  recovery 
of  the   functionally  defective  conduction. 

A  comparison  of  these  two  cases  of  partial  block  represented  in 
Figures  18  and  19  is  interesting.  In  the  first  case  (Figure  18)  the 
auricle  contracts  regularly,  the  ventricle  irregularly.  In  the  second 
case  (Figure  19)  the  auricle  contracts  irregularity,  the  ventricle 
regularly  and  at  a  much  slower  rate  than  in  the  preceding  case.    The 


Bradycardia.     Heart  Block 


47 


Figure  21 

Delayed  conduction.     P-R  interval  =  0.2  second. 


Figure  22 

Delayed   conduction.      P-R    interval  =  0.6   second.     From   the  same   case   as   Figure   z\ 
after  a  considerable  amount  of  digitalis  had  been  given. 


48  Bradycardia.     Heart  Block 

irregularity  in  each  case  is  a  rhythmic  one.  In  the  first  case  a 
regular  auricle  associated  with  a  defect  in  conduction  produces 
a  rhythmic  irregularity  of  the  ventricle.  In  the  second  case  the 
rhythmic  irregularity  of  the  auricle  associated  with  a  defect  in  con- 
duction produces  a  regular  activity  of  the  ventricle. 

The  electrocardiogram  of  a  case  of  complete  block  is  shown  in 
Figure  20.  Here  it  is  to  he  noted  that  the  ventricular  complexes 
(R  S  T)  are  normal  in  form  except  when  they  are  distorted  by 
superimposed  P  waves  which  recur  at  regular  intervals  hut  with 
no  fixed  relation  to  successive  ventricular  complexes.  The  P 
waves  are  equidistant  from  one  another  but  fall  in  any  portion  of 
the  ventricular  cycle  (both  systole  and  diastole).  The  ventricle 
is  contracting  at  the  rate  of  27  and  is  perfectly  regular,  the  auricle 
with  a  slight  arrythmia  contracts  at  a  rate  of  60.  The  activities 
of  the  upper  and  lower  chambers  are  quite  independent.  This 
complete  dissociation  of  auricles  and  ventricles  is  entirely  charac- 
teristic of  complete  block.  No  impulses  can  pass  from  the  auricle 
to  the  ventricle  and  each  has  its  independent  rhythm.  The  pace 
of  the  auricle  is  set  by  the  normal  pacemaker,  the  sinus  node. 
The  ideo-ventricular  pacemaker  is  in  this  case  located  in  the  bundle 
of  His  above  its  bifurcation  (if  the  impulses  which  initiate  the 
contractions  of  the  lower  chamber  were  in  some  other  portion 
of  the  ventricular  musculature,  as  is  sometimes  the  case,  the  ven- 
tricular complexes  would  be  of  an  entirely  different  type). 

Only  those  cases  have  been  described  which  represent  distinct 
types  of  block;  it  should  be  said,  however,  in  passing  that  a 
single  case  may  present  various  degrees  of  block  at  different  times, 
delayed  conduction,  partial  and  complete  block  may  present  them- 
selves in  a  single  case  at  successive  periods  and  more  rarely  one 
may  follow  a  case  passing  through  the  stages  of  complete  and 
partial   block  back   to   a   condition   of   normal  activity. 

A  number  of  the  simpler  and  more  common  types  of  partial 
and  complete  auriculo-ventricular  block  have  been  discussed ;  this 
list,  however,  by  no  means  exhausts  the  varieties  of  heart  block 
which  are  seen  in  the  clinic.  Block  associated  with  sinus  irregu- 
larities, extrasystoles  and  auricular  fibrillation  are  some  of  the 
types  which  will  be  taken  up  in  subsequent  chapters. 

The   differentiation   of    a   block    produced   by   an   organic  lesion 


5o  Bradycardia.    Heart  Block 

from  that  resulting  from  a  hypertonic  condition  of  the  vagus  may 
often  be  made  by  noting  the  effect  of  the  administration  of  atropin. 
In  cases  of  Vagus  block,  the  paralyzing  of  the  terminal  nerve 
endings   with  atropin  abolishes  the  block. 

CLINICAL   FEATURES  AND   SIGNIFICANCE 

The  milder  grades  of  interferences  with  the  property  of  con- 
duction are  often  associated  only  with  those  signs  which  we  have 
described  in  pointing  out  the  means  for  their  clinical  recognition. 
The  patient  may  be  entirely  unconscious  of  any  abnormality  and 
his  attention  may  first  be  called  to  the  condition  by  the  physician 
who  discovers  the  arrhythmia.  While  a  moderate  degree  of  de- 
layed conduction  may  be  accompanied  by  no  other  symptoms,  its 
recognition  and  true  evaluation  is  important,  for  it  means,  as  a 
rule,  intrinsic  myocardial  defect.  This  may  be  either  an  organic 
or  a  chemical  change  in  the  muscle  cells.  It  may  be  permanent 
or  temporary,  but  it  nearly  always  means  some  sort  of  damage  to 
the  slender  bundle  of  muscle  connecting  auricles  and  ventricles.  In 
taking  this  stand,  I  am  quite  aware  that  a  considerable  degree  of 
impaired  conduction  may  be  produced  both  experimentally  and  clin- 
ically by  stimulation  of  the  left  vagus  nerve,  and  yet  I  believe  that 
clinically  these  vagus  effects  are  usually  only  in  evidence  when 
the  tissues  under  their  control  are  functionally  damaged. 

The  recognition  of  this  defect  is  also  important,  because  it  usually 
indicates  extensive  myocardial  change.  It  is  the  most  evident 
feature  because  the  integrity  of  the  A-V  bundle  is  essential  to  the 
sequential  co-ordination  of  auricles  and  ventricles,  and  yet  it  is 
rare  to  find  a  lesion  of  the  bundle  without  other  widespread  dam- 
age in  the  walls  of  both  the  upper  and  lower  chambers.  Indeed, 
it  is  the  rule,  rather  than  the  exception,  that  the  injury  to  the  A-V 
bundle  is  merely  a  part  of  the  pathological  process  involving  a 
large  portion  of  the  heart  muscle. 

The  identification  of  this  defect  is  of  considerable  practical  value, 
since  these  hearts  are  particularly  susceptible  not  only  to  vagus 
influences,  but  also  to  drugs  of  the  digitalis  group.  Some  degree 
of  block  may  often  be  initiated  in  a  normal  heart  by  the  adminis- 
tration of  toxic  doses  of  digitalis.  In  those  showing  an  abnormal 
conduction,  digitalis  is  frequently  a  potent  influence  in  accentuat- 


Bradycardia.    Heart  Block  51 

ing  the  defect.  It  does  not  follow  from  this  that  digitalis  is  always 
eontraindicated  in  conduction  abnormalities.  Some  of  these  pa- 
tients seem  to  improve  when  the  block  is  increased,  but  in  such 
cases  it  should  be  given  with  caution  and  with  a  knowledge  of 
the  effect  which  may  be  expected. 

A  complete  functional  destruction  of  the  bundle  of  His  i  not 
necessarily  followed  by  cardiac  insufficiency.  I  have  had  under  my 
observation  for  the  past  three  years  a  young  woman  referred  to 
me  by  Professor  Janeway,  in  whom  a  complete  heart  block  was 
discovered  during  a  routine  examination.  She  has  at  no  time  given 
any  evidence  of  cardiac  insufficiency  and  during  this  period  has 
completed  a  course  of  training  as  nurse  in  the  Presbyterian  Hos- 
pital, involving  no  small  amount  of  physical  exertion. 

Cardiac  insufficiency  in  cases  of  dissociation  is  more  often  due 
to  the  inability  of  a  damaged  ventricle  to  maintain  its  part,  rather 
than  the  result  of  the  cutting  off  of  the  normal  auricular 
impulses. 

During  the  course  of  acute  rheumatic  fever,  diphtheria,  pneu- 
monia and  other  infectious  diseases,  one  should  be  on  the  outlook 
for  conduction  disturbances.  These  are  met  with  not  only  during 
the  height  of  the  active  process,  but  also  during  convalescence.  I 
have  seen  its  development  on  several  occasions,  some  days  after 
the  defervescence  of  an  acute  lobar  pneumonia,  in  diphtheria  long 
after  the  subsidence  of  the  acute  symptoms,  and  in  rheumatism 
when  the  patient  was  beginning  to  move  about.  Under  these  con- 
ditions the  block  is  frequently  only  a  temporary  affair  and  even- 
tually disappears  with  the  removal  of  the  toxins  and  the  restitution 
of  the  cells  of  the  myocardium.  The  indiscriminate  use  of  digitalis 
in  the  acute  infections  is  to  be  deprecated.  It  may  be  of  great 
service  when  properly  used,  but  may  also  do  distinct  injury  unless 
carefully  adapted  to  the  needs  of  the  individual  patient. 

In  complete  block  the  rate  of  the  ventricle  is  quite  independent 
of  reflex  influences ;  excitement  may  increase  the  auricular  rate  in 
its  accustomed  manner,  but  the  ventricular  rate  is  undisturbed.  The 
same  has  been  noted  in  regard  to  the  effects  of  the  administration 
of  alcohol  and  chloroform  (Mackenzie). 

We  have  discussed  the  cases  of  heart  block  in  which  the 
arrhythmia  is  the  only  symptom  and  in  which  there  is  no  altera- 


52  Bradycardia.     Heart  Block 

tion  in  the  general  blood  distribution,  also  a  group  of  cases  in  which 
the  arrhythmia  may  or  may  not  be  the  only  evidence  of  a  myo- 
cardial lesion,  but  in  which  the  heart  is  unable  to  maintain  an 
adequate  circulation,  with  a  result  that  the  ordinary  symptoms  of 
cardiac  insufficiency  ensue.  In  the  latter  we  conclude  that  there  is 
always  a  defective  ventricular  muscle  in  addition  to  the  abnormal 
condition  of  the  A-V  bundle. 

There  remains  for  our  consideration  a  group  of  cases  which  is 
characterized  by  symptoms  which  are  directly  dependent  upon  the 
arrhythmia  for  their  development.  This  is  the  group  that  has  long 
been  recognized  as  the  Adams-Stokes  syndrome.  Its  distinctive 
features  are  attacks  of  unconsciousness,  with  or  without  convulsive 
movements,  associated  with  a  sudden  slowing  of  the  usual  pulse 
rate.  The  seizures  are  probably  the  result  of  a  sudden  cerebral 
anaemia  attending  the  abrupt  slowing  of  the  left  ventricle.  The 
attacks  may  be  very  infrequent  and  occur  at  intervals  of  months 
or  may  follow  one  another  with  great  rapidity,  so  that  "twenty  to 
thirty"  may  be  counted  in  twenty-four  hours.  They  differ  greatly 
in  their  duration  and  in  their  severity.  Sometimes  the  loss  of  con- 
sciousness is  merely  momentary  or  it  may  be  prolonged  for  sev- 
eral minutes.  The  breathing  may  be  at  first  stertorous  and  be  fol- 
lowed later  by  apnoea,  or  the  respiration  may  be  normal  through- 
out the  attack.  If  the  attack  is  momentary  there  is  usually  a 
pallor  of  the  face;  in  a  prolonged  attack  there  is  venous  congestion 
with  extreme  cyanosis.  The  convulsion  may  consist  of  slight 
twitching  of  the  face  or  of  one  arm  or  in  the  more  severe  parox- 
ysms it  may  become  general.  The  attack  is  usually  ushered  in 
with  a  sudden  decrease  in  the  ventricular  rate  and  with  pauses 
between  the  beats  of  varying  duration.  The  change  may  consist 
in  a  fall  of  rate  from  the  normal  to  the  neighborhood  of  30,  or, 
in  cases  with  a  block  of  considerable  duration  and  an  established 
rate  of  30,  the  rate  may  suddenly  fall  to  7  or  8  per  minute.  Dur- 
ing the  attack  the  veins  of  the  neck  may  be  prominent  and  are 
seen  pulsating  rhythmically  at  the  rate  of  60  or  over  per  minute. 
After  the  attack  the  heart  will  usually  be  found  to  be  beating 
rhythmically  at  about  30  per  minute.  This  sudden  change  in  an 
established  ideo-ventricular  rhythm,  with  its  associated  loss  of  con- 
sciousness, is  additionally  suggestive  of  serious  damage  to  the  veil- 


Bradycardia     Heart  I '.lock  53 

tricular  muscle,  for  a  normal  ventricle  should  maintain  its  ideo- 
ventricular  rhythm  unimpaired. 

The  exciting  cause  of  this  syndrome  is  often  found  in  a  little 
unusually  physical  exertion.  In  extreme  cases,  walking  a  short 
distance  has  been  found  sufficient  to  induce  an  attack,  while  in 
others  a  moderate  amount  of  exertion  is  endured  with  impunity. 

Since  the  ordinary  path  by  which  the  ventricles  are  influenced 
is  severed,  we  do  not  know  the  mechanism  through  which  exercise 
may  affect  them.  It  may  be  by  a  direct  effect  on  the  myocardium 
of  an  altered  blood  supply,  or  possibly  by  reflex  influences  through 
those  few  fibers  of  the  extracardial  nerves  which  are  known  to 
terminate  in  the  ventricular  muscle. 

It  should  always  be  remembered  that  the  terms  heart  block  and 
Adams-Stokes  syndrome  are  not  synonymous.  The  former  desig- 
nates a  dissociated  activity  of  the  auricles  and  ventricles,  and  may 
continue  indefinitely  without  the  attacks  of  cerebral  anjemia  and 
unconsciousness,  which  are  characteristic  of  the  Adams-Stokes 
complex. 

COURSE  AND  PROGNOSIS 

Every  case  of  heart  block,  even  those  of  the  mild  degree  show- 
ing only  a  prolonged  auricu'lo-ventricular  interval  or  occasional 
dropped  beats,  demand  close  observation  over  a  long  period  of 
time.  This  is  not  because  the  defect  in  the  A-V  bundle  is  in  itself 
a  serious  matter,  but  because  it  is  usually  indicative  of  more  ob- 
scure and  more  extensive  lesions  of  the  other  parts  of  the  myo- 
cardium, and  because  it  often  affords  the  earliest  evidence  of  a 
functional  impairment  which  is  progressive.  It  is  rarely  the  only 
evidence  of  heart  damage;  usually  one  finds,  in  addition,  a  valvular 
defect,  signs  of  a  pericarditis,  dilatation,  hypertrophy,  or  other 
direct  evidences  of  more  extensive  myocardial  damage. 

A  mild  degree  of  the  depression  of  conduction  in  itself  rarely 
induces  cardiac  insufficiency,  but  aside  from  the  concomitant 
lesions  which  may  be  present  and  which  have  been  referred  to 
above,  such  hearts  have  a  "margin  of  safety"  under  the  normal. 
In  my  experience  a  very  large  proportion  of  hearts  which  show 
this  abnormality  during  the  course,  or  subsequent  to  the  acute  mani- 
festations of  influenza,  pneumonia  or  typhoid  fever,  entirely  recover 


34  Bradycardia.     Heart  Block 

their  normal  function.  When  the  defect  follows  diphtheria,  rheuma- 
tism  or  a  syphilitic  infection,  it   is  more  apt   to  he  permanent. 

The  prognosis  in  these  mild  types  depends  primarily  on  the  func- 
tional condition  of  the  heart,  aside  from  the  arrhythmia  due  to 
the  injury  to  the  bundle.  If  the  lesion  of  the  bundle  is  stationary, 
and  if  it  is  the  only  evidence  of  cardiac  damage,  it  may  he  re- 
garded with  little  apprehension.  Patients  do  not  die  of  mild  degrees 
of  heart  block,  nor  is  the  reserve  force  of  the  heart  greatly  re- 
duced thereby. 

Unfortunately,  in  a  considerable  number  of  instances,  a  per- 
sistent heart  hlock  shows  itself  to  be  part  of  a  progressive  lesion. 
Symptoms  of  ventricular  damage  gradually  develop  or  the  evidences 
of  bundle  defect  gradually  or  abruptly  indicate  a  transition  to  a 
more  severe  type  of  abnormal  function. 

It  is  at  the  time  of  the  sudden  change  from  a  mild  degree  of 
block  to  the  more  severe  grades  that  the  attacks  of  unconscious- 
ness and  convulsions,  which  are  characteristic  of  the  Adams-Stokes 
syndrome,  are  wont  first  to  appear.  The  cerebral  anaemia  seems 
to  be  induced  by  the  sudden  transition  from  the  faster  to  the  slow 
rate.  'When  the  block  becomes  complete  and  the  lower  chamber 
takes  on  its  slow  rhythmic  ideo-ventricular  rhythm,  there  is  less 
liability  to  these  seizures.  Later  there  may  be  other  abrupt  falls 
in  rate  (manifestly  due  to  defects  of  the  ventricular  myocardium) 
and  once  more  the  attacks  of  unconsciousness  appear  with  renewed 
severity  and   frequency. 

A  severe  grade  of  heart  block  is  a  serious  condition.  It  is  usually 
associated  with  widespread  myocardial  damage  and  consequent 
cardiac  insufficiency.  The  latter  is  most  commonly  the  cause  of 
the  gradual  incapacitating  of  the  patient  and  ultimately  of  his 
death.  That  these  associated  conditions  are  usually  the  factors  of 
moment  is  evidenced  by  the  fact  that  one  sees  cases  of  complete 
block  who  for  years  follow  their  accustomed  activities  unconscious 
of  any  abnormal  circulatory  condition  and  are  incommoded  only 
when  other  evidences  of  myocardial  change  appear. 

The  development  of  fits,  which,  however,  occurs  in  only  a  small 
percentage  of  those  afflicted  with  heart  block,  is  a  grave  sign.  The 
first  attack  may  be  fatal  and  the  only  prodrome  recognized  may 
have  been  a  slow  or  irregular  heart  action.     More  commonly  the 


Bradycardia.     Heart  Block  55 

patient  has  a  number  of  attacks  often  with  very  little  apparent 
harm.  The  attacks  once  established  are  prone  to  recur  at  shorter 
intervals  and  with  increasing  severity.  One  cannot  predict  when 
a  seizure  is  likely  to  prove  fatal.  Even  the  majority  of  those  who 
develop  the  Adams-Stokes  syndrome,  however,  do  not  die  in  one 
of  the  attacks.  They  are  far  more  apt  to  succumb  to  a  gradually 
increasing  cardiac  insufficiency  terminating  in  heart  failure  with- 
out cerebral  symptoms. 

Prognosis,  on  the  whole,  should  rest  on  a  study  of  the  extent 
and  progress  of  the  myocardial  defect  and  an  estimate  of  the  ven- 
tricular efficiency.  Few  patients  survive  the  inception  of  attacks 
of  cerebral  anaemia  more  than  two  or  three  years.  The  end  may 
come  at  any  time.  Exceptionally  the  duration  of  life  is  longer. 
Several  of  Edes'  cases  lived  seven  or  eight  years  after  the  onset 
of  the  Adams-Stokes  syndrome.  A  case  reported  by  Osier  lived 
thirty  years  after  the  discovery  of  brachycardia  and  seven  years 
after  the  first  syncopal  attack.  Gerhardt  has  reported  three  cases 
in  which  syncopal  attacks  and  heart  block  completely  disappeared. 


CHAPTER  VII 

The  Extxasystole 

In  the  routine  examination  of  the  pulse  our  attention  is  frequent- 
ly attracted  by  a  form  of  irregularity  which  has  the  following  char- 
acters:  the  rhythm  is  for  longer  or  shorter  periods  that  of  a  normal 
pulse,  but  at  intervals  this  rhythm  is  interrupted  by  a  pause  during 
which  one  may  get  the  impression  that  one  pulse  beat  has  failed  in 
its  normal  sequence;  it  appears  as  if  one  pulse  beat  had  been  omitted 
and  the  impression  is  often  described  as  "a  dropped  beat"  or  as  "an 
intermittent  pulse."  When  we  come  to  verify  our  impressions  by 
more  careful  observation  we  may  find  that,  during  this  pause  in 
which  we  at  first  thought  a  beat  had  been  missed,  v%'e  are  able  to 
detect  on  delicate  palpation,  a  small  pulse  wave  which  had  at  first 
escaped  our  attention ;  this  wave  is  usually  much  smaller  than  the 
waves  of  the  normal  rhythm  ;  it  occurs  at  a  time  which  is  a  little 
too  early  for  the  occurrence  of  a  beat  of  the  normal  rhythm  and  is 
followed  by  a  pause  which  is  somewhat  greater  than  the  inter- 
val between  the  beats  of  the  normal  rhythm ;  this  pause  is  usu- 
ally followed  by  a  pulse  wave  which  is  a  little  larger  and  more 
forcible  than  the  waves  of  the  normal.  This  irregularity  is  known 
as  an  cxtrasystole.  It  is  evidently  the  result  of  a  ventricular  con- 
traction which  has  occurred  too  early  and  which  is  less  forcible  than 
the  normal  rhythmic  contractions  of  the  heart;  it  is  therefore  also 
known  as  premature  contraction.  On  auscultating  such  a  heart  we 
will  detect  a  rhythmic  series  of  normal  sounds  interrupted  at  inter- 
vals by  a  group  of  sounds  which  are  weaker  and  occur  earlier  than 
those  of  the  normal  cycles;  this  first  and  second  sounds  of  the  weak 
group  are  followed  by  a  silence  which  is  considerably  longer  than 
the  normal  diastolic  period. 

In  some  of  the  hearts  of  this  group  the  extrasystolic  contraction 
will  be  represented  by  a  single  sound  only,  and  no  corresponding 
wave  even  of  an  abortive  character  can  be  detected  in  the  peripheral 
arteries.  These  signs  indicate  that  the  premature  beat  was  wanting 
in   force  sufficient  to  open  the  aortic  valve.     The  question  of  the 

56 


The  Extrasystole  57 

opening  of  the  aortic  valve  depends  on  three  factors :  (a)  the  energy 
of  the  premature  ventricular  contraction;  (b)  the  volume  of  the 
blood  in  the  ventricle  at  the  moment;  and  (c)  the  blood  pressure 
in  the  aorta.  These  factors  depend  in  turn  upon  the  time  of  the 
occurrence  of  the  extrasystole.  If  this  comes  early  in  diastole 
the  contractile  power  of  the  ventricle  will  have  recovered  to  only 
a  moderate  degree;  the  volume  of  blood  in  the  ventricle  will  then 
be  small  and  the  aortic  pressure  will  be  near  its  highest  point ;  hence 
it  is  hardly  probable  that  the  aortic  valves  will  be  opened  and  such  a 
premature  contraction  will  be  accompanied  by  the  first  heart  sound 
only;  the  second  sound,  due  to  the  closure  of  the  aortic  valve,  will 
be  absent  and  there  will  be  no  corresponding  pulse  wave.  If.  how- 
ever, the  extrasystole  comes  later  in  the  diastolic  period,  contrac- 
tility will  have  more  completely  recovered ;  the  volume  of  blood 
which  has  passed  into  the  ventricle  will  be  greater  and  the  aortic 
pressure  to  be  overcome  much  less ;  hence  the  aortic  valve  will  be 
opened;  the  second  heart  sound  will  be  heard  and  the  small  extra- 
systolic  wave  may  be  felt  at  the  wrist. 

PATHOLOGY  AND   ETIOLOGY 

In  the  sections  on  the  physiology  of  the  heart  it  was  pointed  out 
that  all  portions  of  the  musculature  of  the  heart  have  the  property 
of  excitability,  that  is  that  any  muscle  cell  can  respond  to  stimuli  at 
any  time  except  during  the  "refractory  period"  which  lasts  for  a 
short  time  after  the  cell  has  been  stimulated.  Also  that  normally 
stimuli  are  rhythmically  originated  at  the  "sinus  node"  and  sweep 
over  the  tissues  of  the  heart  in  an  orderly  manner,  exciting  to 
activity  its  chambers  in  a  definite  sequence. 

If  electrical  stimuli  of  the  proper  strength  be  applied  by  means 
of  suitable  electrodes  to  the  wall  of  the  heart  of  the  experimental 
animal  (frog,  turtle  rabbit,  dog,  etc.),  it  will  respond  by  a  contrac- 
tion, no  matter  what  portion  of  the  musculature  is  excited ;  the  ac- 
tivity thus  produced  will  spread  downward  in  the  direction  taken 
by  physiological  stimuli  and  also  from  the  point  of  stimulation  up- 
ward toward  the  sinus  node,  i.e.,  in  a  direction  the  reserve  of  that 
of  physiological  stimuli,  and  the  chambers  of  the  heart  will  contract 
in  the  order  in  which  the  stimuli  reach  them.  Contractions  thus 
excited  from  an  abnormal  focus  are  known  as  extrasystoles,  and, 


58  TlIF.    E.XTR ASYSTOLE 

according  to  their  point  of  origin,  are  known  as  auricular,  ventric- 
ular, etc. 

If,  in  this  manner,  the  heart  is  systematically  studied  by  applying 
stimuli  in  the  various  phases  of  the  cardiac  cycle  while  the  heart  is 
beating  rhythmically,  it  will  be  found  that  for  a  period  beginning 
just  before  and  extending  a  short  time  after  systole,  the  heart  is  not 
excitable  even  by  very  powerful  stimuli,  i.e.,  the  heart  is  in  the  "re- 
fractory phase"  because  the  molecules  upon  which  the  fundamental 
properties  of  cardiac  muscle  depend  have  been  decomposed  into  their 
constituent  ions.  Now  the  extrasystole  which  has  been  experimen- 
tally produced  throws  the  heart  muscle  into  the  "refractory  phase" 
so  that  the  next  physiological  stimulus  of  the  rhythmic  series  aris- 
ing at  the  sinus  node  will  reach  the  muscle  cells  lower  down  when 
they  are  inexcitable,  hence  it  will  be  ineffective  in  producing  a 
systole.  The  next  systole  will  not  occur  until  it  is  brought  into  being 
by  the  next  spontaneous  stimulus  which  is  formed  at  the  sinus  node 
and  which  occurs  exactly  at  the  moment  at  which  it  would  have 
occurred  had  there  been  no  extrasystole.  This  lengthened  diastolic 
period  which  follows  the  extrasystole  is  known  as  the  "compensatory 
pause."  When  the  time  consumed  between  the  last  normal  heart 
beat  preceding  the  extrasystole  and  the  normal  beat  following  the 
compensatory  pause  is  exactly  equal  to  the  time  occupied  by  two 
beats  of  the  normal  rhythm,  the  long  diastolic  pause  following  the 
extrasystole  is  known  as  a  "complete  compensatory  pause;"  when 
the  interval  between  the  last  spontaneous  systole  and  the  post-com- 
pensatory systole  is  less  than  the  interval  between  two  systoles  of 
the  normal  rhythm,  the  compensatory  pause  is  called  "incomplete." 

A  study  of  the  compensatory  pause  in  the  mammalian  heart  re- 
veals the  following  facts:  (a)  When  the  sinus  node  is  stimulated 
the  extrasystole  is  not  followed  by  a  compensatory  pause,  (b) 
When  the  auricle  is  stimulated  the  compensatory  pause  is  usually 
incomplete,  (c)  When  the  ventricle  is  stimulated  the  compensatory 
pause  is  complete.  These  facts  may  be  explained  on  the  following 
grounds :  As  soon  as  the  stimulus  material  at  the  node  is  destroyed 
by  its  direct  stimulation,  the  construction  of  the  material  is  immedi- 
ately recommenced  and  reaches  the  explosive  point  at  an  interval 
just  equal  to  the  period  of  the  normal  rhythm.  When  the  auricle 
is  stimulated  early  in  the  diastolic  period  (see  Figure  26)  the  stim- 


The  Extk asystole 


5'J 


V, 


^^^ 


X 


Figure  26 

Kxtrasystole  arising  from   the   auricle    near   the   sinus. 


s 


s    \    \    \ 


5 


AH 


EB 


Figure  27 

Extrasystole  arising  from   a  point  low  down  in   the  auricle. 


Ay 


'1  '1  1  j    -i  -i  '1  '1  i^i 


Figure  28 

Extrasystole  arising  from  a  point  in  the  ventricle. 

Diagrams  to  illustrate  the  mechanism  of  the  extrasystole  starting  from  various  parts 
of  the  heart  muscle.  The  arrows  indicate  the  points  of  origin  and  the  directions  taken 
by  the  stimuli.  Dotted  arrows  indicate  the  time  at  which  the  normal  stimulus  at  the  sinus 
node  should  reach  maturity  if  its  formation  was  not  interrupted  by  the  extrasystole. 
The  thickness  of  the  lines  representing  ventricular  systole  indicate  the  relative  effect  of 
the  normal  beat  and  the  extrasystole  in  maintaining  an  adequate  circulation.  As  =  auricu- 
lar systole.     A-V  =  auriculo-ventricular  bundle.     Vs  —  ventricular  systole. 


6o  The  Extrasystole 

ulllS  is  conveyed  not  only  to  the  ventricle  but  also  upward  to  the 
node  and  will  destroy  the  spontaneously  forming  stimulus  material 
at  the  node  before  it  has  reached  the  explosive  point,  hence  the 
interval  between  the  last  physiological  stimulus  and  the  post-extra- 
systolic  stimulus  will  be  somewhat  less  than  two  cycles  of  the  normal 
rhythm.  When  the  auricular  stimulation  occurs  somewhat  later 
in  diastole  the  retrograde  stimulus  may  reach  the  node  coincident 
with  the  explosion  of  the  rhythmically  formed  stimulus  material, 
hence  in  this  instance  the  post-extrasystolic  pause  will  be  fully  com- 
pensatory. When  the  ventricle  is  stimulated  (see  Figure  28)  the 
retrograde  stimulus  reaches  the  sinus  node  during  its  refractory 
period  just  after  its  physiological  stimulus  and  the  post-extrasys- 
tolic stimulus  will  exactly  equal  the  period  between  two  beats  of  the 
normal  rhythm  and  the  post-extrasystolic  pause  will  be  fully  com- 
pensatory. This  explanation  indicates  how  extrasystoles  arising 
from  different  parts  of  the  auricles  may  have  compensatory  pauses 
either  complete  or  incomplete.  It  may  be  stated,  as  a  general  rule, 
that  the  nearer  to  the  sinus  node  is  the  point  of  stimulation  initiating 
an  extrasystole,  and  the  earlier  it  occurs  in  diastole,  the  shorter  will 
be  the  post-extrasystolic  pause ;  and,  conversely,  the  farther  from 
the  sinus  node  is  the  point  of  origin  of  the  extrasystole  and  the  later 
it  occurs  the  more  nearly  will  the  post-extrasystolic  pause  be  com- 
pensatory. 

Electrocardiographic  studies  have  further  shown  that  the  stimuli 
originating  extrasystoles  may  pass  over  the  musculature  of  the  heart 
by  the  normal  paths  (nomodrome  extrasystole),  or,  since  the  stim- 
uli may  originate  from  some  point  far  removed  from  the  normal 
path  or  may  be  shunted  from  this  path  by  abnormal  conditions  of 
the  muscles  which  form  an  obstruction  to  their  passage,  they  may 
take  an  unusual  course  through  the  cardiac  tissue  (allodrome  extra- 
systoles). A  discussion  of  these  abnormal  paths  and  their  varie- 
gated but  characteristic  electrocardiographic  records  will  be  left  for 
a  later  paragraph. 

Extrasystoles  have  been  produced  experimentally  in  many  ways 
other  than  the  employment  of  electrical  stimuli.  Mechanical  irrita- 
tion, heat,  the  application  of  irritating  salts,  obstruction  of  the  great 
veins  (Stassen),  clamping  of  the  aorta  (Hering),  ligation  of  a 
branch  of  the  coronary  artery    (Lewis),  the  injection  of   digitalis 


The  Extrasystole  6i 

and  atropin  (Cushny),  adrenalin  (Kahn),  muscarine  and  physo- 
stigmine  (Rothbcrgcr  and  Winterbcrg).     Under  proper  conditions 

extrasystoles  have  been  produced  in  the  isolated  perfused  heart  and 
in  the  mammalian  heart  in  situ  after  all  nervous  connections  have 
been  severed,  hence  it  is  probable  that  their  cause  is  an  increased 
excitability  of  the  muscle  cells  usually  quite  independent  of  nervous 
influences,  though  Kraus  and  Nicolai  have  produced  them  by  vagus 
irritation. 

The  conditions  of  the  experimental  production  of  extrasystoles 
have  been  set  forth  at  some  length  since  it  is  upon  inferences  from 
these  data  that  our  conception  of  the  pathological  conditions  under- 
lying the  extrasystole,  as  met  with  in  man,  is  based.  Very  little 
indeed  is  known  of  the  histological  changes  associated  with  the  pro- 
duction of  extrasystoles  and  there  still  remains  here  a  field  for  care- 
ful and  exhaustive  research.  Clinically  extrasystoles  are  found  far 
more  frequently  in  those  with  slow  hearts  and  often  they  may  be 
made  to  disappear  by  moderate  exercise  which  quickens  the  heart 
rate.  The  experimental  evidence  seems  to  indicate  clearly  that  the 
extrasystole  occurs  because  some  cardiac  muscle  cells  become  more 
excitable  than  those  of  the  sinus  node  and  it  is  therefore  on  this 
ground,  easy  to  understand  why  an  increase  in  excitability  should 
be  more  apparent  during  a  slow  rate,  since  in  the  faster  rates 
the  excitability  of  the  node  is  greater  than  in  the  slow  rates ;  under 
such  conditions  the  abnormal  irritability  of  some  portion  of  the 
auricle  or  ventricle  must  be  considerable  to  make  itself  evident. 

It  also  seems  fair  to  assume  from  the  experimental  evidence  that 
nutritional  disturbance  may  play  an  important  part  in  increasing  the 
excitability  of  heart  muscle;  an  atheroma  with  a  narrowing  of  the 
coronary  artery  or  one  of  its  branches  may  be  the  pathological 
counterpart  of  the  ligation  of  the  branches  of  the  coronary  which 
has  been  shown  by  Lewis  to  regularly  produce  extrasystoles. 

Numerous  toxic  agents  are  known  to  be  associated  with  the  pro- 
duction of  extrasystoles ;  they  are  quite  common  in  many  febrile 
conditions,  notably  in  acute  rheumatic  fevers.  One  of  the  very 
common  phenomena  produced  by  the  administration  of  large  doses 
of  digitalis  (at  least  to  patients  having  damaged  hearts)  is  the  ap- 
pearance of  ventricular  extrasystoles ;  on  the  withdrawal  of  this 
drug  they  disappear.     Nicotine  is  another  of  the  cardiac  poisons 


62  The  Extrasystole 

which  is  clinically  prominent  as  a  cause  of  extrasystoles.  The  "to- 
bacco heart"  is  one  in  which  premature  beats  have  become  so 
frequent  as  to  make  themselves  uncomfortably  evident.  Excessive 
tea  drinkers  are  subject  to  this  form  of  irregularity.  Premature 
beats  are  found  in  persons  of  all  ages ;  they  are  rare  in  the  first  dec- 
ade of  life  and  are  most  common  after  the  age  of  50.  They  are 
considerably  more  common  among  men  than  among  women. 

Extrasystoles  are  probably  very  much  more  common  than  is  gen- 
erally supposed;  it  has  been  estimated  that  a  majority  of  persons 
reaching  middle  age  have  had  extrasystoles  at  some  period.  They 
are  frequently  met  with  in  those  who  afford  other  signs  of  impair- 
ment of  the  heart,  such  as  valvular  disease,  myocardial  degeneration 
and  the  cardiac  complications  of  nephritis,  but  premature  contrac- 
tions are  also  not  uncommonly  found  in  those  whose  hearts  have 
no  discoverable  abnormality  other  than  this  irregularity. 

Premature  contractions  are  exceedingly  common  in  individuals 
of  the  neurotic  type;  they  may  sometimes  be  induced  by  irritation 
of  the  skin  and  in  persons  subject  to  this  irregularity,  merely  plung- 
ing the  hands  into  cold  water  is  sufficient  to  develop  it.  They  are 
often  associated  with  digestive  disturbances,  particularly  when  ac- 
companied by  flatulency.  As  has  been  mentioned  exercise  will  fre- 
quently cause  the  temporary  disappearance  of  extrasystoles,  but  if 
carried  to  the  point  of  fatigue  the  irregularity  is  prone  to  become 
more  evident  than  before.  In  those  predisposed  to  them,  suspen- 
sion of  respiration  for  a  few  seconds  will  sometimes  induce  these 
premature  contractions.  When  present  in  the  upright  position  they 
will  often  disappear  as  soon  as  the  subject  lies  down,  even  though 
this  change  in  position  is  accompanied  by  a  slight  diminution  in  the 
rate  of  the  heart.  Extrasystoles  are  quite  common  during  convales- 
cence from  infectious  diseases. 

IDENTIFICATION 

Clinically,  the  starting  point  for  establishing  the  presence  of  the 
extrasystole  is  to  determine  whether  the  patient  has  a  fundamentally 
normal  cardiac  rhythm,  which  is  broken  on  occasions  more  or  less 
frequently.  When  the  interruptions  occur  at  infrequent  intervals,  as 
is  the  case  in  the  majority  of  these  patients,  the  detection  of  the 
fundamental   rhythm  is  comparatively  easy.     If  one  palpates  the 


Tin-:  Kxtkasystoi.k  63 

radial  artery  there  arc  long  periods  during  which  the  pulse  is  per- 
fectly regular,  then  occasionally  this  regular  rhythm  is  broken  by 
a  pause  which  is  too  long  to  fit  the  fundamental  rhythm,  or  one 
may  detect  a  very  small  pulse  wave  followed  by  a  pause  longer  than 
that  ordinarily  separating  the  waves  of  the  normal  rhythm.  When 
one  listens  to  the  heart  sounds  they  will  be  heard  for  long  periods 
as  a  normal  rhythmic  scries  until  this  series  is  broken  by  the  occur- 
rence of  one  or  two  indistinct  heart  sounds  which  follow  the  last 
normal  sounds  too  early  and  which  arc  in  turn  followed  by  a  pause 
longer  than  that  occupied  by  the  interval  between  the  heart  sounds 
of  the  periods  of  normal  rhythm.  The  small  premature  waves  de- 
tected in  the  radial  and  the  indistinct  premature  first  for  first  and 
second)  sounds  heard  over  the  precordium,  each  followed  by  a 
more  or  less  complete  compensatory  pause,  are  our  usual  common 
evidences  of  the  presence  of  extrasystoles.  Whether  one  hears  at 
the  time  of  the  premature  beat  a  first  and  second  heart  sound  or  only 
a  first  heart  sound  depends,  as  has  been  pointed  out  in  a  preceding 
paragraph,  on  whether  the  extrasystolic  contraction  has,  or  has  not 
opened  the  aortic  and  pulmonary  valves. 

If  murmurs  are  present  during  the  periods  of  normal  rhythm, 
they  are  much  less  distinct  in  the  premature  cycle  and  may  be  ab- 
sent. The  mitral  systolic  is  the  murmur  which  can  most  easily  be 
detected  in  the  extrasystolic  cycle;  the  presystolic  is  more  rarely 
heard ;  while  aortic  murmurs  are  absent  or  shortened  in  consonance 
with  the  action  of  the  valve  which  may  fail  to  open,  or  open  only 
for  a  brief  period.  I  have  recently  seen  a  case  presenting  extra- 
systoles  in  which  no  heart  sounds  could  be  heard,  both  first  and  sec- 
ond sounds  being  replaced  by  loud  harsh  murmurs.  At  the  time 
of  the  extrasystole  one  could  hear  four  murmurs  following  each 
other  at  equally  spaced  intervals.  The  first  and  second  of  these 
murmurs  were  louder  and  a  little  longer  than  the  third  and  fourth ; 
the  fourth  murmur  was  followed  by  a  considerable  pause  which  was 
succeeded  by  a  repetition  of  the  two  murmurs  which  constituted  the 
auscultatory  evidence  of  the  ordinary  rhythmic  activity  of  the  heart. 

Another  type  of  rhythm  which  is  easily  recognized  as  due  to 
extrasystoles  is  the  so-called  "bigeminus."  Here  the  radial  pulse 
shows  a  rhythmic  series  composed  of  a  large  wave,  a  short  pause, 
a  small  wave  and  a  long  pause.     This  sequence  is  repeated  again 


t>4  The  Extrasystole 

and  again.  Tlie  repeated  recurrence  of  two  pulse  waves  followed 
by  a  pause  has  given  rise  to  the  very  expressive  term  "coupled 
rhythm."  It  consists  of  a  wave  of  the  fundamental  rhythm  fol- 
lowed by  a  premature  beat  and  its  compensatory  pause.  This 
rhythm  is  one  of  the  common  manifestations  of  toxic  doses  of 
digitalis.  When  an  extrasystole  occurs  every  third  heat  it  gives 
rise  to  a  rhythm  that  was  formerly  described  as  the  "pulsus 
trigeminus." 

When  extrasystoles  occur  quite  frequently  and  at  very  irregular 
intervals  it  is  sometimes  more  difficult  to  assure  oneself,  by  the  ordi- 
nary physical  signs,  that  the  irregularity  is  due  to  premature  con- 
tractions, but  careful  observation  will  usually  discover  a  fundamen- 
tal rhythm,  interrupted  by  beats  which  occur  too  early,  are  followed 
by  a  pause  and  each  time  they  appear  give  the  impression  of 
"coupling." 

Inspection  of  the  jugular  pulse  is  frequently  an  aid  in  making  the 
diagnosis  of  an  extrasystole.  The  two  venous  waves  which  one 
ordinarily  sees  during  the  fundamental  rhythm  are  often  replaced 
at  the  time  of  the  premature  contraction  by  a  single  venous  wave 
larger  than  the  others.  This  wave  is  due  to  the  inability  of  the  vein 
to  discharge  its  contents  into  the  auricle  at  this  moment,  since  the 
pressure  in  the  auricle  is  abnormally  high,  the  ventricle  being  in 
systole  and  the  auriculoventricular  valves  being  closed.  This  is,  of 
course,  more  in  evidence  when  the  origin  of  the  extrasystole  is  in 
the  ventricular  wall  and  the  auricle  and  ventricle  contract  simul- 
taneously. 

Whether  an  extrasystole  is  auricular  or  ventricular  in  origin  can 
only  be  definitely  decided  by  graphic  records  and  yet  the  trained 
observer  who  has  sharpened  his  powers  of  differentiation  by  corre- 
lating his  physical  signs  with  the  evidence  of  the  graphic  records, 
can  often,  by  noting  the  length  of  the  compensatory  pause  and  the 
character  of  the  heart  sounds  of  the  premature  beat,  quite  correctly 
assign  a  particular  extrasystole  to  its  proper  category. 

A  graphic  record  of  the  radial  or  of  the  apex  beat  is  often  suffi- 
cient evidence  to  establish  the  presence  of  the  extrasystole.  Such 
a  record  (Figures  30,  31  and  32)  shows  a  series  of  similar  waves  re- 
curring at  equal  intervals.  This  rhythm  is  more  or  less  frequently 
interrupted  by  a  small  wave  which  occurs  too  early  to  fit  into  the 


'I  HE    EXTRASYSTOLE 


65 


0.2  second 


Figure  29 

Auricular  extrasystole  at  x.     The  compensatory  pause  is  incomplete. 


Brachial 


1.2  second 


Figure  30 

Auricular   extrasystole    at   x.      a'    of   extrasystole    superimposed   on    preceding   r    wave. 
The  compensatory  pause  is  incomplete. 


66  The  Extrasystole 

fundamental  rhythm.  It  is  followed  by  a  pause  longer  than  that 
between  two  bleats  of  the  fundamental  rhythm,  which  in  turn  is 

followed  by  a  wave  which  is  usually  a  little  larger  than  the  average 
wave  of  the  rhythmic  series  and  which  is  the  first  of  a  new^  series 
of  rhythmic  waves.  In  the  case  of  an  extrasystole  which  originates 
in  the  ventricle  the  post-cxtrasystolic  pause  is  fully  compensatory 
(see  Figures  32  and  33).  When  the  extrasystole  has  its  origin 
higher  up  in  the  cardiac  tissues,  the  pause  i>  "incomplete"  (  Figures 
Jo,  30  and  31  ).  The  reason  for  this  has  been  explained  in  a  pre- 
ceding paragraph    (page  (>o). 

THE  POLYGRAM 

Auricular1  Extrasystoles.  The  jugular  tracing  throws  additional 
light  on  the  mechanism  (Figures  29  and  30).  Figure  29  shows  a 
rhythmic  series  of  waves  a  c  i\  which  is  several  times  (at  x)  inter- 
rupted by  a  similar  group  which  occur  too  early;  it  is  clear  that  the 
auricle  contracts  too  soon  and  is  followed  by  a  sequential  contrac- 
tion of  the  ventricle. 

Another  case  of  auricular  extrasystole  is  shown  in  Figure  30; 
here  the  premature  contraction  of  the  auricle  occurs  earlier  in  the 
cycle  than  was  the  case  in  Figure  29,  so  that  the  auricular  premature 
wave  a'  is  superimposed  on  the  v  wave  of  the  preceding  group;  the 
simultaneous  contraction  of  the  ventricle  and  the  auricle  causes  an 
unusual  temporary  stasis  in  the  jugular  vein,  hence  this  large  wave 
(v  a'),  The  extrasystole  is  followed  by  a  compensatory  pause  which 
is  "incomplete." 

The  Nodal  Extrasystole  is  illustrated  (x  Figure  31).  In  this  in- 
stance our  conception  is  that  the  premature  contraction  starts  at  a 
point  in  the  tissues  junctional  between  auricles  and  ventricles ;  from 
this  point  the  stimulus  sweeps  upward  to  the  auricle  and  downward 
to  the  ventricle  so  that  these  chambers  contract  practically  simultane- 
ously, hence  the  waves  a'  and  c'  of  the  jugular  coincide.  The  retro- 
grade stimulation  of  the  auricle  has  destroyed  the  usual  stimulus 
material  accumulating  at  the  normal  pacemaker ;  the  building  up  of 
stimulus  material  is,  however,  at  once  recommenced  and  this  reaches 
maturity  in  the  normal  time  which  is  shown  by  the  fact  that  the 
time  elapsing  between  the  wave  a'  of  the  extrasystole  and  the  suc- 
ceeding a  wave  is  exactly  the  interval  of  the  normal  rhythmic  series. 


'I  in.    I'..-.  I  RASYSTOLE 


67 


%c     **.  S'  fc 


*r5v 


■ 


j  \ 


Radial 


JUJlLLUlUJUJlLLUJuJUUlJlUUl^ 


Figure  31 

Nodal  extrasystole  at  x.     In  the  jugular  tracing  the  a  and  c  waves  of  the  extrasystole 
occur  simultaneously.     The  compensatory  pause  is  incomplete. 


Jugular 


Brachial 


0.2  second 


Figure  32 
Ventricular  extrasystole  at  x.     In  the  extrasystolic  cycle  the  auricle  and  ventricle  con- 
tract simultaneously  (a' c').     The  compensatory  "pause  is  complete. 


68  The  Extrasystole 

Ventricular  Extrasystoles  are  shown  in  Figure  32.  The  auricle, 
as  represented  by  the  a  waves  of  the  jugular  record,  contracts  rhyth- 
mically, but  occasionally  (x)  the  ventricle  contracts  prematurely  so 
that  at  these  times  the  auricle  and  ventricle  contract  simultaneously 
and  their  activities  are  represented  by  a  large  wave  (a'  c')  in  the 
jugular  tracing.  The  absence  of  the  v  wave  in  the  extrasystolic 
cycle  which  is  quite  evident  in  the  records  is  due  to  the  empty  con- 
dition of  the  ventricle  at  the  time  of  the  premature  contraction.  It 
is  to  be  noted  that  the  post-extrasystolic  pause  is  fully  compensa- 
tory. Figure  33,  with  its  diagrammatic  analysis,  shows  a  ventricular 
extrasystole  which  occurs  every  thin  beat  giving  rise  to  the  so- 
called  "pulsus  trigeminus." 

Mixed  types  of  extrasystoles  are  not  infrequently  seen  in  a  single 
case.  A  tracing  of  such  a  patient  is  shown  in  Figure  34.  Here  one 
may  make  out  the  following  sequence:  normal  beat,  auricular  extra- 
systole, ventricular  extrasystole.  The  analysis  of  the  polygraph  in 
these  cases  is  sometimes  quite  difficult.  The  analysis  of  the  tracing 
shown  in  Figure  34  was  subsequently  verified  by  electrocardio- 
graphic records  in  which  the  analysis  is  much  less  difficult. 

THE  ELECTROCARDIOGRAMS 

As  a  rule  the  identification  of  the  kind  and  point  of  origin  of  the 
extrasystole  is  most  accurately  made  by  means  of  the  electrocardi- 
ographic record.  The  most  distinctive  features  of  extrasystoles  are 
that  (1)  they  occur  too  early,  and  (2)  they  are  followed  by  a  pause 
greater  than  the  normal  intersystolic  pause. 

To  fix  clearly  the  phenomena  which  the  electrocardiogram  dis- 
closes, upon  which  we  base  conclusions  as  to  the  point  of  origin  of 
the  extrasystole,  let  us  recall  just  what  the  movements  of  the  string 
of  the  galvanometer  represent.  At  any  given  moment  the  deflection 
of  the  string  indicates  the  algebraic  sum  of  the  differences  of  elec- 
trical potential  of  the  heart  as  a  whole.  When  the  stimulus  arises 
at  the  sinus  node  (the  normal  pacemaker)  and  passes  over  the  heart 
in  a  sequential,  orderly  manner,  a  series  of  deflections  occur  which 
we  have  learned  to  recognize  (see  Chapter  IV)  as  the  normal  differ- 
ences of  electrical  potential  for  successive  instants  of  the  cardiac 
cycle.  If  now  the  stimulus  arises  from  some  point  of  the  cardiac 
musculature  other  than  the  "sinus  node"  it  is  quite  evident  that  the 


TlUi   EXTRASY!  I  "i.i. 


bg 


0.2  second 


Figure  33 

'Pulsus  trigeminus"  due  to  an  cxtrasystole,  which  occurs  every  third  beat. 


Ventricular     and    auricular 
a'  c'  —  auricular  extrasystole. 


Figure  34 

extrasystoles    in    a    single    record. 
"  —  ventricular  extrasystole. 


Jugular 


Brachial 


;cond 


a  C  =^  normal     cycle, 


yo  The  Extrasystole 

impulse  passing  by  abnormal  paths  and  reaching  purl  ions  of  the 
cardiac  tissues  at  intervals  quite  at  variance  with  the  normal  will 
produce  differences  of  electrical  potential  at  successive  moments  of 
the  cardiac  cycle  quite  different  from  the  normal.  How  great  are 
the  variations  in  electrical  potential  which  result  from  the  extra- 
systolic  contractions  may  best  be  appreciated  by  a  study  of  the 
curves  which  are  here  reproduced. 

Auricular  Extrasystoles.  When  the  focus  from  which  the  extra- 
systole  arises  is  at  or  near  the  sinus  node  the  electrocardiographic 
complexes  are  usually  of  the  normal  form.  Such  a  record  is  shown 
in  Figure  35.  It  is  composed  of  a  series  of  complexes,  each  of  which 
is  practically  of  the  normal  type.  Each  cycle  is  opened  by  a  P  wave, 
which  at  its  proper  interval  is  followed  by  a  normal  ventricular  com- 
plex, Q  R  S  T.  In  the  center  of  the  record  the  fundamental  rhythm 
is  broken  by  a  cycle  ( x )  which,  although  normal  in  other  respects, 
occurs  prematurely  and  is  followed  by  a  pause  which  is  not  quite 
long  enough  to  be  completely  compensatory.  This  premature  con- 
traction must  have  arisen  at  or  near  the  sinus  node,  since  the  vari- 
ous parts  of  the  cardiac  musculature  have  been  stimulated  by  paths 
and  in  a  sequence  which  is  the  normal  one. 

The  curve  reproduced  in  Figure  36  shows  an  extrasystole  which 
has  arisen  high  up  in  the  auricle  near  the  sinus.  Here  the  extrasys- 
tole has  occurred  so  early  that  its  P  wave  is  superimposed  on  the  T 
wave  of  the  preceding  cycle  producing  a  wave  which  is  equal  to  P  -f- 
T.     The  pause  following  the  extrasystole  is  incomplete. 

It  has  been  shown  by  Lewis*  that  if  the  auricle  of  an  animal 
is  made  to  contract  by  applying  artificial  stimuli  to  various  portions 
of  the  auricular  tissue,  the  resulting  electrocardiographic  records 
will  be  greatly  modified.  When  the  point  of  stimulation  is  at  or 
near  the  sinus  node  the  P  wave  is  upward  in  direction  and  of  a  form 
which  we  have  come  to  regard  as  normal;  as  the  point  of  stimula- 
tion is  made  more  and  more  remote  from  the  sinus  the  P  complexes 
become  irregular  in  form  and  may  be  directed  downward  or  show 
a  diphasic  variation.  We  are  therefore  led  to  infer  that  in  the 
human  electrocardiogram  an  upward  single  P  wave  represents  an 
auricular  contraction  originating  at  or  near  the  sinus  node;  a  down- 
ward directed  P  wave  indicates  an  origin  in  the  lower  part  of  the 

♦Heart,  iqio,  ii,  27. 


The  Extrasystole 


7i 


ifyl  P  T         P      '      T     P  T  p  T  ;• 


Figure  35 

Auricular  extrasystole  at  x.     Compensatory  pause   incomplete.     P  —  auricular  contrac- 
tion.     R-T  =  ventricular   contraction.      Brachial    tracing   above. 


Figure  36 

Auricular  extrasystole  at  x.     The  auricular  wave  P  of  this  extrasystole  is  superimposed 
on   the    T  wave   of  the  preceding  ventricular   complex. 


Figure  37 

Extrasystole  at  x  arising  from  a  point  low  down  in  the  auricle.     P  is  directed  down- 
ward in  the  extrasystole.     P  following  extrasystole  is  diphasic.     Below  is  brachial  tracing. 


Figure  38 

"Pulsus  trigeminus"  caused  by  an  auricular  extrasystole,  which  occurs  every  third  beat 
at  x.  P  is  reversed  in  extrasystole,  indicating  a  point  of  origin  low  down  in  auricle. 
Radial   tracing  above. 


72  The  Extrasystole 

auricle ;  a  notched  or  diphasic  P  wave  indicates  an  intermediate 
point  of  auricular  origin. 

An  extrasystole  which  arose  in  the  lower  part  of  the  auricular 
tissue  is  shown  in  Figure  37.     The  complexes  of  the  ordinary  rhythm 

are  normal  in  form  except  that  the  P  waves  arc  rather  too  broad 
and   have   summits  which  are  slightly   flattened;   the   extrasystolic 

cycle  (  x  )  is  initiated  by  a  P  wave  which  is  directed  downward  but 
is  followed  by  a  ventricular  complex  which  is  normal  in  form,  indi- 
cating that  the  ventricular  response  to  the  premature  auricular 
activity  was  the  result  of  an  impulse  which  passed  down  through 
the  A-V  bundle  and  over  the  ventricular  musculature  by  the  normal 
paths  in  a  perfectly  orderly  manner.  It  may  he  noted  in  passing 
that  the  auricular  complex  which  immediately  follows  the  extrasys- 
tole has  a  form  somewhat  different  from  the  P  waves  of  the  suc- 
ceeding normal  cycles ;  this  is  not  an  unusual  occurrence  and  sug- 
gests that  the  auricle  has  not  as  yet  entirely  recovered  its  normal 
function. 

Figure  38  displays  a  rhythm  which  was  formerly  known  as  the 
"pulsus  trigeminus."  It  consists  of  a  series  of  two  normal  beats  fol- 
lowed by  an  auricular  extrasystole.  The  impression  produced  on 
the  palpating  finger  by  a  pulse  of  this  type  is  indicated  by  the  radial 
curve  taken  simultaneously  with  the  electrocardiogram.  All  the 
auricular  (P)  complexes  of  this  record  show  an  unusual  diphasic 
form,  suggesting  that  even  those  impulses  which  originated  at  the 
sinus  node  have  taken  an  abnormal  path  through  the  auricular 
tissue.  The  P  waves  of  the  extrasystole  (.r)  are  clearly  reversed, 
indicating  an  origin  low  down  in  the  auricle. 

The  ventricular  extrasystole  presents  in  the  electrocardiogram 
(Figure  41),  a  complex  far  removed  from  that  of  the  normal  ven- 
tricular contraction.  The  abnormal  point  of  origin  and  the  conse- 
quent abnormal  path  which  the  impulse  follows  usually  produces  a 
much  greater  difference  of  electric  potential  than  does  the  impulse 
which  descends  from  the  auricle  and  follows  the  normal  path 
through  the  A-V  bundle  and  its  branches.  The  auricle  contracts  at 
regular  intervals,  so  that  often  when  an  extrasystole  occurs  the 
ventricular  and  auricular  contractions  are  simultaneous.  The  little 
wave  representing  auricular  activity  wilf  then  occur  during  the  time 
of  ventricular  activity  and  is  usually  relatively  so  small  that  it  is 


Jul  Extras^  tole 


d^'t^i^^F^ 


Figure  39 

Lead    II.      Every  P  wave  is  of  an  abnormal   form   indicating   an   abnormal    point    of 

origin    in    the    auricle    or   an   abnormal    path    through    the   auricular   wall. 


Figure  40 

Auricular  extrasystoles   from   a  point  low   down  in  the  auricle.     Xote   the  short  PR 
interval   of   the  extrasystoles   and   the    incomplete   compensatory    pauses. 


Lead  I 


Lead  II 


Lead  III 


J^JU&jJ&U^h  Jt^Jwto^yfc^  i 


Figure  41 

Ventricular  extrasystole  at  x  arising  from  a  point  at  the  base  of  the  left  ventricle 
Showing  similarity  in  the  complexes  obtained  by  leads  II  and  III.  Compare  P  R  T  =  nor 
mal  complex  and  extrasystolic  complex  x. 


74 


The  Extrasystole 


submerged  in  the  large  waves  of  the  ventricular  complex.  Figure 
41  shows  an  electrocardiogram  taken  from  a  patient  by  the  cus- 
tomary three  leads.  The  first  and  last  complexes  of  each  lead  are 
the  normal  for  this  individual,  between  these  are  seen  the  cxtrasys- 
toles.  It  is  to  be  noted  that  the  form  of  the  extrasystolic  waves 
are  very  similar  in  leads  II  and  III,  but  that  these  differ  very  ma- 
terially from  the  extrasystole  pictured  in  lead  I.  The  similarity  of 
form  of  the  extrasystolic  complexes  of  leads  II  and  III  is  usual.  The 
complex  of  lead  I  may  be  similar  in  form  to  that  of  lead  II,  but  it 
is  usually  quite  different.  The  submerged  auricular  wave  which 
occurs  during  the  extrasystole  can  be  seen  (only  in  lead  II)  as  a 
small  notch  (P)  in  the  final  dip  of  the  extrasystolic  complex. 

Systematic  studies  of  the  electrical  complexes  obtained  by  stimu- 
lating various  portions  of  the  right  and  left  ventricles  both  when  the 
branches  of  the  bundle  of  His  are  intact  and  when  one  of  the 
branches  has  been  cut,  have  shown  that  a  comparison  of  the  re- 
cords* taken  by  lead  I  and  lead  II  will  indicate  the  point  from 
which  the  extrasystole  has  its  origin. 

The  prominent  types  are  shown  in  Figures  42,  43,  44  and  45.  The 
direction  of  the  principal  deflection  in  leads  I  and  II  with  the  points 
of  origin  of  the  extrasystoles  may  be  tabulated  as  follows : 


TYPE 

DIRECTION  OF  PRINCIPLE 
DEFLECTION 

POINT  OF    ORIGIN    OF 
STIMULUS. 

LEAD    I. 

LEAD  II. 

1 
0 

3 

4 

up 

up 
down 
down 

up 

down 
up 

down 

Right  ventricle  near  base 

"             "      apex 

Left    ventricle  near  base 

apex 

A  type  of  curve  which  is  not  infrequently  met  with  is  shown  in 
Figure  46.  Two  ventricular  extrasystoles  appear  in  this  record. 
Each  is  preceded  by  a  P  wave  which  occurs  at  its  regular  rhythmic 

*Rothberger  and  Winterberg:  Archiv.  fur  die  ges.  Physiologic,  1913,  cliv, 
P-  571- 


I.ra.l      I 


Lead  if 


75 


*.*■«*  ^y^it^^f^  ^r^r* 


Figure  42 

Type.    1.      Ventricular   extrasystole    arising   from   a  point   in    the   right   ventricle    near 
the  base. 


h^rfrf-*^ 


Figure  43 

Type   2.      Ventricular  extrasystole  arising  from  a  point  in  the  right  ventricle  near   the 
apex.     Above  brachial  tracing  the  extrasystole  produces  no  arterial   wave. 


Figure  44 

Type  3.     Ventricular  extrasystole  arising  from  a  point  in  the  wall  of  the  left  ventricle 
near  the  base.     Radial  tracing  above. 


Figure  45 

Type  4.     Ventricular  extrasystole  arising  from  a  point  in  the  wall  of  the  left  ventricle 
near  the  apex. 


-6  The  Extrasystole 

interval.  At  first  sight  one  might  regard  this  as  an  impulse  which 
had  its  origin  in  the  auricle  and  which  was  shunted  off  by  an  ab- 
normal  path  through  the  ventricular  wall.  One  notices,  however, 
that  the  length  of  the  P-R  interval  of  the  normal  complexes  is  unusu- 
ally long  (over  0.2  second),  while  the  interval  between  /'  and  the 
onset  of  the  extrasystolic  complex  is  very  brief  (0.1  second).  It  is 
therefore  evident  that  insufficient  time  has  elapsed  between  P  and 
the  onset  of  the  extrasystole  to  permit  of  the  passage  of  the  stimulus 
from  the  auricle  to  the  ventricle,  and  we  must  conclude  that  the 
ventricle  has  contracted  in  response  to  a  stimulus  initiated  independ- 
ently in  its  own  wall. 

A  contrast  to  this  case  is  shown  in  Figure  47.  Here  the  ventric- 
ular extrasystole  (at  x)  occurs  relatively  early  and  the  auricular 
contraction  P  is  seen  as  a  step  on  the  descending  limb  of  the  large 
extrasystolic  wave.  The  arterial  tracing  which  accompanies  this  as 
well  as  many  of  the  preceding  electrocardiograms  shows  the  rela- 
tively small  wave  which  is  produced  in  the  arterial  tree  by  the  extra- 
systole. This  evident  lack  of  efficiency  of  the  premature  contraction 
in  maintaining  an  adequate  circulation  is  due  to  two  factors  (1)  the 
abnormal  sequence  of  the  stimulation  of  the  muscle  fibers  of  the 
ventricle  results  in  a  contraction  which  is  relatively  incoordinated, 
and  the  propelling  power  of  the  ventricles  is  less  than  under  the 
normal  conditions;  (2)  on  account  of  the  prematurity  of  its  contrac- 
tion the  ventricle  is  less  well  filled  with  blood,  hence  a  smaller 
volume  is  expelled  into  the  aorta. 

The  nodal  extrasystole.  The  majority  of  extrasystoles  which  one 
sees  in  the  clinic  have  their  origin  in  some  portion  of  the  ventricular 
wall.  Auricular  premature  contractions  are  far  less  frequent.  A  still 
more  rare  form  of  extrasystole  is  shown  in  Figure  48.  In  this  curve 
the  extrasystolic  complex  is  only  slightly  changed  from  the  ventri- 
cular complex  of  the  fundamental  rhythm,  the  following  pause  is 
fully  compensatory  and  the  presence  of  P  in  its  normal  rhythmic 
position  following  the  principal  wave  of  the  extrasystole  shows  that 
the  rhythm  of  the  auricle  has  not  been  disturbed.  Since  the  ven- 
tricular portion  of  the  extrasystolic  complex  has  a  form  not  unlike 
the  ventricular  complexes  of  the  sequential  rhythm  and  yet  clearly 
is  not  the  result  of  auricular  activity,  we  conclude  that  its  point  of 
origin  is  at  some  point  high  up  in  the  auriculo-ventricular  bundle 


The  Extrasystole 


77 


Figure  46 

Ventricular  extrasystole  at  x.     The  auricle  contracts  rhythmically,  as  shown  by  P  waves. 
P-R   interval  =  0.3   second.     The   extrasystole   does  not   originate   in   the   auricle. 


2 


7»        t 


,.  ..  x  » 


^^-^^^ 


Figure  47 

Ventricular  extrasystole  at  x,  showing 
submerged  P  waves.  Brachial  tracing  above. 
Extrasystolic  pause  is  fully  compensatory. 


Figure  48 

Nodal  extrasystole  at  x.  At  time  of  ex- 
trasystole auricle  and  ventricle  contract  si- 
multaneously. Origin  of  ventricular  im« 
pulse  is  high   up   in   the  A-V  bundle. 


^S  The  Extr  vsystole 

anil  that  Its  subsequent  course  through  the  ventricular  wall  follows 
the  normal  channels.     This  is  known  as  the  nodal  extrasystole. 

The  interpolated  extrasystole  is  another  rare  form  of  premature 
contraction.  An  extrasystole  always  ventricular  in  origin  occurs 
between  two  beats  of  the  normal  rhythm  without  otherwise  disturb- 
ing the  orderly  course  of  either  the  auricular  or  the  ventricular 
rhythm   (  Figures  40.  50  and  511. 

In  Figures  52  and  53  are  shown  two  types  of  "pulsus  bigeminus," 
each  due  to  an  alternation  of  normal  cardiac  contractions  and  extra- 
systoles;  the  extrasystoles  of  Figure  52  arise  in  the  wad  of  the  right 
ventricle  near  the  apex;  the  premature  contractions  of  Figure  53 
arise  in  a  point  in  the  left  ventricular  tissues  near  its  base. 

Extrasystoles  of  different  points  of  origin  frequently  are  met  with 
in  the  same  patients  on  separate  occasions  and  sometimes  in  close 
succession.  Figure  54  shows  auricular  extrasystoles  at  A  and  ven- 
tricular extrasystoles  at  x.  The  auricular  extrasystoles  have  an  in- 
complete, the  ventricular  a  complete  compensatory  pause.  Figure  55 
shows  an  alternation  of  ventricular  extrasystoles  (x)  and  normal 
ventricular  complexes.  At  the  center  of  the  record  (  Y)  the 
quence  is  further  disturbed  by  the  occurrence  of  a  ventricular  extra- 
systole from  an  entirely  new  point  of  origin. 

THE    CLINICAL    SIGNIFICANCE 

of  the  extrasystole  is  one  of  considerable  importance.  Most  of  us 
have  followed  the  career  of  patients  who  have  had  occasional  extra- 
systoles for  a  number  of  years  and  often  we  can  secure  a  history  of 
the  existence  of  this  form  of  irregularity  for  many  years,  antedating 
our  own  observations,  yet  we  rarely  see  a  case  of  cardiac  insuffi- 
ciency which  can  reasonably  be  attributed  to  this  irregularity 
per  sc.  The  patient  is  often  quite  conscious  of  what  they 
often  describe  as  a  "thumping"  in  the  precordial  region,  "fluttering 
of  the  heart,"  or  "palpitation."  On  examination  a  large  number  of 
these  sensations  can  be  shown  to  be  due  to  the  presence  of  extra- 
systoles. These  sensations  are  often  the  occasion  of  considerable 
alarm  to  the  patient  particularly  when  they  are  first  discovered  and 
the  physician  who  assures  them  that  this  irregularity  in  itself  is  of 
very  little  significance  and  rarely  is  the  forerunner  of  more  serious 


The  Extrasystole 


79 


R 


UAmw^^A> 


Ai 


H 


Figure  49 

Interpolated  extrasystole. 


Figure  50 

Patient     G.       Lead     I.         Interpolated    extrasystole    at    X.       Ventricular     extrasystole 
type  i. 


Figure  51 

Patient    G.      (same   as    Figure    50.)      Lead    II.      Interpolated    ventricular    extrasystole 
type  1. 


80  The  Extrasystole 

trouble  docs  the  patient  a  great  service  in  removing  his  grounds  for 
anxiety. 

When,  however,  we  see  cases  which  show  extrasystoles  at  very 
frequent  intervals  and  particularly  when  the  extrasystoles  arise 
from  more  than  one  focus  our  prognosis  should  be  much  more 
guarded,  such  irregularities  are  evidences  of  more  serious  myocardial 
defects.  The  rapid  and  persistent  increase  in  the  number  and  a 
multiplication  of  the  foci  of  origin  of  extrasystoles  point  to  advanc- 
ing myocardial  changes  and  are  often  associated  with  symptoms  in- 
dicating cardiac  insufficiency.  Curiously  enough  some  of  the  pa- 
tients in  whom  I  have  discovered  extrasystoles  occurring  constantly 
and  in  great  numbers  were  quite  unconscious  of  cardiac  irregular- 
ities. 

A  more  prolonged  study  of  the  different  types  of  extrasystoles, 
their  points  of  origin  and  their  frequency  may  eventually  lead  us  to 
modify  our  prognosis  in  accordance  with  such  findings,  but  as  yet 
our  facts  do  not  warrant  more  positive  statements.  Our  prognosis 
ultimately  rests  on  the  extent  of  myocardial  damage,  and  the  extra- 
svstole  is  merely  one  of  the  symptoms  which  suggest  that  the  de- 
fective muscle  is  little  or  much  affected. 


The  Extrasystole 


Hi 


Figure  52 

"Bigeminus."     The  extrasystoles  (x)   arise   from  the  wall  of  the  right  ventricle   n<  ar 

the  apex   (Type  2). 


Figure  53 

"Bigeminus."     The  extrasystoles  (x)  arise  from  a  point  in  the  wall  of  the  left  ventricle 
near  the  base  (Type  3). 


Figure  54 
Extrasystoles  from  different  points  of  origin.     A  =  auricular  extrasystole  with  incom- 
plete compensatory  pause.     X  =  ventricular  extrasystoles  with  complete  compensatory  pause. 


tW ^>*W '#{*«*'&*  ^■«* ***'  ^-AwirtW*/', 


^KH*'^W  ^»^»  *^'  fj***^ 


%        Y 


Figure  55 

Two  types  of  ventricular  extrasystoles.      X   arising  from   the   right  ventricle  near  the 
base.     Y  arising  from  the  left  ventricle  near  the  apex  (Types  1  and  4). 


CHAPTER  VIII 

Tachycardia 

A  heart  rate  of  abnormal  rapidity  is  one  of  the  most  frequent  phe- 
nomenon observed  by  the  physician.  For  purposes  of  the  present 
discussion  one  may  classify  all  such  cases  in  two  groups  : 

I.    ACCELERATED    HEARTS. 
II.    PAROXYSMAL  TACHYCARDIA. 

The  main  clinical  feature  which  distinguishes  these  groups  is  the 
manner  in  which  the  transition  from  the  normal  to  the  abnormal 
rate  is  accomplished.  In  the  case  of  the  accelerated  heart  the  transi- 
tion from  the  slow  to  the  rapid  and  from  the  rapid  to  the  slow  rate 
is  gradual ;  in  a  very  brief  period  the  heart  cycle  may  become  so 
shortened  that  the  rate  per  minute  is  increased  50  per  cent.,  and  yet, 
as  observed  by  palpation  or  auscultation,  the  length  of  any  two  suc- 
cessive cycles  is  so  nearly  identical  that  neither  the  finger  nor  the 
ear  is  able  to  detect  the  minute  differences  which  go  to  make  up  the 
change. 

In  the  paroxysmal  tachycardia  the  onset  and  the  offset  of  the 
change  in  rate  is  abrupt  and  the  observer  and  even  the  patient  is 
usually  able  to  detect  the  sudden  transition  without  difficulty. 

THE  ACCELERATED  HEART 
ETIOLOGY  AND  PATHOLOGY 

It  has  already  been  pointed  out  that  the  rate  of  the  normal  heart 
is  not  fixed,  but  varies  with  the  needs  of  the  body  at  any  particular 
moment.  This  rate  adjustment  is  brought  about  through  the  regula- 
tory mechanism  of  the  extra  cardial  nerves.  In  the  conditions  now 
to  be  considered  the  underlying  factors  are  many  and  complicated, 
but  we  may  recognize  three  important  elements  which  individually 
or  in  association  may  produce  an  abnormal  acceleration  of  the  heart: 

(A)    The  outside  demands  on  the  heart  may  be  excessive. 

A  full  discussion  of  the  demands  on  the  heart  which  originate 
outside  of  the  cardio-regulatory  nervous  mechanism  and  the  cardiac 


Tachycardia  83 

tissues  themselves,  the  nature  of  such  demands  and  their  modus 
operandi,  important  and  interesting  as  they  arc,  would  had  us  out- 
side of  the  limits  which  we  have  set  in  these  chapters  devoted  to  the 
suhject  of  myocardial  function.  However,  this  outside  call  for  in- 
creased cardiac  activity  must  never  be  lost  sight  of  in  analyzing  the 
response  of  the  cardiac  tissues  to  these  demands.  A  simple  illustra- 
tion of  the  response  of  the  heart  to  increased  demand  is  seen  in  the 
effect  of  work.  As  a  general  rule  it  may  be  stated  that  the  response 
to  physical  exertion  of  an  individual  with  a  good  myocardium  is 
shown  in  an  increased  blood  pressure.  One  with  a  defective  myocar- 
dium shows  an  abnormal  acceleration  of  the  heart  rate.  With  a 
normal  heart  muscle  under  efficient  regulation  and  a  normal  vaso- 
motor tone,  moderate  exercise  causes  an  increase  of  cardiac  rate, 
but  with  rest  the  rate  should  return  to  its  usual  level  in  the  space  of 
a  very  few  minutes.  That  the  demands  of  exercise  produce  an  in- 
trinsic physiological  effect  on  the  myocardium  is  evidenced  by  the 
fact  that  the  normal  electrocardiogram  constantly  shows  under  such 
stress  definite  though  small  changes ;  in  addition  to  the  shortening  of 
the  diastolic  period  (T-P)  there  is  an  increase  in  the  size  of  waves 
P  and  T  and  a  deepening  of  S\ 

(B)  The  extracardial  nerves  may  be  at  fault  in  their  regulatory 
capacity. 

It  is  quite  evident  in  certain  accelerated  hearts  that  the  fine  nervous 
adjustments  are  unbalanced.  The  activity  of  the  vagi  are  depressed 
or  there  is  an  excessive  activity  of  the  accelerators,  such  a  lack  of 
balance  mainly  affects  the  heart  through  its  pacemaker,  the  sinus 
node.  This  is  probably  the  mechanism  of  the  rapid  changes  of  rate 
in  emotional  conditions,  the  so-called  "labile  pulse"  of  neurasthenics 
and  the  more  persistent  rate  increase  in  certain  organic  lesions  of  the 
central  nervous  system  and  of  the  peripheral  nerves  supplying  the 
heart. 

(C)  The  heart  muscle  may  be  defective  and  responds  to  normal 
outside  demands  with  abnormal  acceleration.  The  direct  application 
of  heat  to  the  myocardium  is  known  to  increase  the  cardiac  activity. 
Bacterial  and  chemical  toxins  set  free  in  many  of  the  infectious  dis- 
eases are  recognized  as  efficient  agents  in  causing  functional  or 
organic  changes  of  the  myocardium,  which  are  the  basis  of  a  response 
in  rate  out  of  proportion  to  the  stress. 


84  Tachycardia 

While  we  can  sometime?  designate  one  of  these  particular  factors, 
excessive  outside  demands,  defective  nerve  regulation  or  myocardial 
damage,  as  the  cause  of  the  increased  heart  rate,  the  problem  is  usu- 
ally more  complicated.  No  doubt  frequently  two  or  all  of  these  ele- 
ments play  a  part.  In  the  present  state  of  our  knowledge  we  are 
often  at  a  loss  in  deciding  which  link  in  the  chain  is  at  fault,  and,  if 
more  than  one,  their  relative  importance. 

Fever  is  nearly  always  accompanied  by  an  acceleration  of  heart 
rate,  and  so  uniform  is  this  phenomenon  that  the  well-known  Lieber- 
meister's  rule  of  an  increase  of  8  pulse  beats  for  each  degree  of  tem- 
perature above  the  normal  is  found  approximately  accurate,  albeit, 
with  many  exceptions.  Whether  this  is  brought  about  by  the  in- 
creased temperature  of  the  blood  passing  through  the  heart,  or  by  the 
chemical  action  of  associated  toxins  on  the  regulatory  nervous 
mechanism,  or  on  the  cells  of  the  cardiac  muscle,  is  undecided. 

The  increased  heart  rate  of  shock  is  undoubtedly  due  to  local  or 
general  vaso-motor  disturbance  with  its  reflex  demands  on  the  heart 
to  maintain  an  adequate  blood  pressure.  A  similar  explanation 
seems  probable  for  Graves'  disease,  and  the  excessive  administration 
of  thyroid  extract  in  which  the  evidence  points  to  the  damaging  effect 
of  toxins  on  the  vaso-motor  apparatus,  rather  than  the  heart  muscle. 
The  "labile  pulse,"  wide  pulse  pressure,  flushing,  local  sweating  and 
tremors  characteristic  of  this  disease  suggest  that  the  toxins  chiefly 
attack  the  sympathetic  nervous  system,  possibly  incidentally  produc- 
ing a  hypertonus  of  the  accelerator  nerves,  and  probably  act  on  the 
heart  muscle  only  in  an  indirect  manner.  Pregnancy  probably  has 
only  a  reflex  effect  on  cardiac  activity. 

Exhausting  diseases  (tuberculosis,  etc.)  and  convalescence  from 
wasting  diseases  (typhoid,  etc.),  nearly  always  show  some  degree  of 
increase  pulse  rate.  Each  one  of  these  conditions,  febrile  or  afe- 
brile, with  toxic  and  nutritional  disturbances  may  affect  the  outside 
demands  on  the  heart,  the  functional  balance  of  the  extracardial 
nerves,  or  the  cardiac  muscle,  and  in  each  instance  the  effort  should 
be  made  to  determine  and  apportion  the  relative  responsibility  of 
each  of  these  factors  in  the  acceleration  of  the  heart.  The  severe 
anemias,  high  grades  of  chlorosis,  marked  secondary  anemias  (as 
in  malignant  disease),  and  the  primary  pernicious  forms  are  in- 
variably associated  with  an  increase  in  heart  rate.     In  the  extreme 


Tachycardia  85 

grades  of  anemia  the  cardiac  muscle  shows  an  advanced  degree  of 
degeneration  with  fatty  infiltration  and  hemorrhages,*  so  thai 
have  little  hesitancy  in  ascribing  the  altered  heart  activity  to  the 
direct  toxic  or  nutritional  effect  on  the  myocardium. 

In  valvular  disease  the  mechanical  defect  must  he  considered.  The 
volume  output  is  unusual  and  the  normal  bodily  calls  for  blood  are 
met  by  an  increased  heart  rate.  In  the  majority  of  these  cases,  how- 
ever, the  disease  which  was  the  agent  in  distorting  the  valves  has 
also  injured  the  myocardium  and  this,  in  association  with  the  change 
in  cardiac  tone  resulting  from  dilatation  and  hypertrophy,  are  impor- 
tant influences  in  modifying  heart  rate.  Changes  in  the  myocardium 
are  produced  by  acute  rheumatic  fever  and  other  infections  diseases 
with  a  resulting  acceleration  of  heart  rate.  These  changes  may  be 
chemical  with  no  demonstrable  histological  abnormality,  or  there  may 
be  fatty  degeneration  and  fibrous  replacement,  so  that  we  meet  with 
many  degrees  of  functional  impairment. 

MECHANISM 

The  main  link  in  the  mechanism  through  which  the  increased  rate 
of  the  "accelerated  heart"  is  produced  is  the  "sinus  node,"  the  nor- 
mal pacemaker  of  the  heart.  Here  the  fundamental  properties  of 
"stimulus  formation"  or  "excitation"  or  both,  become  heightened. 
This  change  may  be  intrinsic,  that  is  to  say,  the  chemical  processes 
of  the  muscle  cells  of  the  node  are  so  changed  that  they  form  and 
explode  stimulus  material  more  rapidly,  or  the  change  may  be 
brought  about  by  the  modifying  impulses  showered  on  the  node  by 
the  extracardial  nerves.  The  sinus  node  is  particularly  influenced  by 
impulses  brought  to  it  by  the  right  vagus  and  the  right  accelerator,  v 

The  distinguishing  feature  of  the  "accelerated  heart"  is  that  the 
sinus  node  retains  its  function  as  the  pacemaker  of  the  heart.  This 
is  shown  by  the  graphic  records  which  indicate  that  the  impulse  for- 
mation arises  at  the  normal  point  and  spreads  through  the  auricle,  the 
bundle  of  His  and  the  ventricle  in  a  normal  orderly  fashion.  There 
are  several  facts,  however,  which  indicate  that,  in  these  "accelerated 
hearts"  other  portions  of  the  musculature  may  have  their  properties 
of  "stimulus  formation,"  "excitability,"  and  perhaps  also  "conduc- 

*Lazarus  :  "Pernicious  Anemia,"  Nothnagel's  Practice,  Phila.,  1906,  p.  283. 
fRobinson  and  Draper:  Jour.  Exp.  Med.,  191 1,  xiv,  p.  227. 


86  TAcm  CARDIA 

tion"  heightened!  It  is  known  that  the  fibers  of  the  left  vagus  and 
of  the  left  sympathetic  are  in  the  main  distributed  to  portions  of  the 
heart  below  the  sinus  node.f  and  experimental  evidence  indicates  thai 
cutting  the  left  vagus  and  stimulating  the  left  sympathetic  have  a 
considerable  effect  in  increasing  the  heart  rate.  Again  in  certain 
"accelerated  hearts"  it  may  be  seen  that  systole,  which  in  the  normal 
heart  has  a  very  constant  length,  is  shortened.  This  is  onlv  con- 
ceivable on  the  ground  that  one  or  more  of  the  fundamental  proper- 
ties of  cardiac  muscle  mentioned  above  are  quantitatively  changed. 

The  principal  change  from  the  normal  in  the  cardiac  cycle  of  the 
accelerated  heart  is  a  shortening  of  the  diastolic  period.  From  this 
it  follows  that  the  rest  period  of  the  heart  is  curtailed  and  the  time 
allowed  for  the  recovery  of  the  property  of  "contractility"  is  con- 
siderably less  than  in  the  heart  working  at  the  normal  rate,  hence  the 
contractile  power  is  less.  Furthermore  there  is  less  opportunity  for 
the  heart  to  receive  its  normal  quota  of  blood,  hence  the  volume  out- 
put is  smaller.  It  follows  as  a  result  of  these  two  factors  that  the 
pulse  is  smaller  in  volume  and  of  diminished  force. 

IDENTIFICATION 

Little  need  be  said  of  the  clinical  recognition  of  the  "accelerated 
heart ;"  the  pulse  may  be  counted  either  by  palpation  at  the  wrist  or 
perhaps  more  accurately  by  auscultation  at  the  apex.  If  one  is  pres- 
ent during  the  change  from  a  slow  to  a  faster  rate  this  is  best  detected 
by  counting  the  pulse  in  10  second  intervals,  omitting  every  other  10 
seconds.  Neither  the  finger  nor  the  ear  can  detect  the  small  differ- 
ences in  the  lengths  of  the  successive  diastolic  periods,  but  the  varia- 
tions in  length  of  the  cycles  separated  by  considerable  periods  is 
easily  made  out.  The  volume  output  of  the  heart  is  usually  some- 
what diminished  with  the  acceleration  of  the  rate  and  the  consequent 
diminution  in  the  peripheral  arterial  wave  may  be  quite  evident. 

The  polygram  of  the  accelerated  heart  conforms  to  the  normal 
except  that  the  diastolic  period  is  shortened.  This  is  at  times  so 
marked  that  the  a  wave  may  be  superimposed  on  the  preceding  v 
wave.  The  jugular  tracings  (  Figures  56  and  57)  show  a  normal  se- 
quence of  waves,  a,  c,  v.  Figure  56  is  a  record  of  a  girl,  15  years  of 
age,  suffering  from  rheumatic  myocarditis  and  adherent  pericardium. 

tCohn  and  Lewis:  Jour.  Exp.  Med.,  1913,  xviii,  p.  739. 


ACM  Y<  IARD1  A 


*7 


Jugular 


Brachial 


0.2  second 


Figure  56 

Accelerated  heart.     Rate  145.    Patient  suffering  from  rheumatic  myocarditis. 


C  '  C    O    p   *"    c  h 


Jugular 


Z~t">U:c\ 


Brachial 


0.2  second 


Figure  57 
Accelerated   heart.      Rate    138.      Case   of    Graves'   disease. 


NX  T  U   HYl  AklMA 

The  rate  at  the  time  the  record  was  taken  was  145  and  the  rapidity 
was  in  part  due  to  excitement,  as  hef  pulse  at  rest  was  commonly  120. 
The  slightest  physical  exertion  at  this  time  would  send  her  pulse  to 
160,  suggesting  a  marked  instability  of  the  sinus  nodi'. 

In  Figure  ?y  is  shown  a  tracing  of  a  ease  of  (iraves'  disease;  tin- 
rate  is  138.  It  is  evident  from  the  jugular  tracing  that  the  normal 
pacemaker  is  in  control  and  that  the  rapid  rate  depends  upon  the 
shortening  of  the  diastolic  period. 

Electrocardiograms  of  accelerated  hearts  are  presented  in  Figures 
58  and  59.  Figure  58,  from  a  case  of  Oaves'  disease,  shows  a  short 
diastolic  period,  hut  the  sequence  of  waves  is  normal.  Figure  59  was 
ohtained  from  a  case  of  cerebral  hemorrhage,  a  few  hours  hefore 
death.  The  diagnosis  was  confirmed  by  autopsy  and  it  seems  clearly 
a  case  in  which  the  nervous  regulatory  mechanism  is  at  fault.  The 
P  and  T  waves  in  this  record  overlap.  Careful  measurement  sug- 
gests that  the  earlier  of  the  two  peaks  represents  the  auricular  con- 
traction which  occurs  before  the  preceding  ventricular  systole  is  com- 
pleted. This  curve  simulates  quite  closely  the  records  obtained 
experimentally  during  the  stimulation  of  the  right  sympathetic  gan- 
glion by  Rothherger  and  Winterberg.* 

Till-:    CLINICAL    SIGNIFICANCE    AM)    PROGNOSIS 

of  the  accelerated  heart  depend  on  the  underlying  condition  and  to 
determine  this,  the  responsibility  of  excessive  outside  demands,  lack 
of  balance  between  the  elements  of  the  nerve  regulatory  mechanism 
and  defects  of  the  myocardium,  must  be  correctly  apportioned.  In 
general  one  may  say  that  excessive  outside  demands  and  unbalanced 
nerve  control  acting  on  a  heart  with  its  myocardium  intact,  are  usu- 
ally more  readily  corrected,  and  hence  of  less  serious  import  to  the 
patient  than  when  the  heart  acceleration  depends  upon  an  intrinsic 
defect  of  the  myocardium.  But  even  a  normal  myocardium  may  be 
worn  out  by  the  excessive  activity  induced  by  extracardial  condi- 
tions, and  a  defective  myocardium  properly  handled  may  recover 
full  functional  efficiency.  The  tests  by  which  we  may  gauge  the 
integrity  of  the  heart  muscle  and  its  reserve  force  will  be  discussed 
in  a  later  chapter. 

♦Archiv.   f.  (1.  ges.  Physiol.,  1910,  exxxv.  p.  557,  Fig.  18,  d. 


Tachycardia 


89 


•L^r 


St+Lu. P  -      *-- 


"'  JJL'^'*     '^ 


«         »  1  '  '  •  »  '-  ».  -^        »         .'.   1 


Ftgure  58 

Accelerated    heart.      Rate    148.     Case  of   Graves'   disease. 


— 


fj     H      IK 


Pt'  pt 


t    - 1- 


^    Sfe    *IF    s|™    «l^ 


tf 


n%^W 


i 


Figure  sq 
Accelerated  heart.     Rate   184.     Terminal  tachycardia  of  cerebral  hemorrhage. 


CHAPTER   IX 

Paroxysmal  Tachycardia 

Acceleration  of  the  heart  rate,  which  lias  been  discussed  in  the 
preceding  chapter,  is  exceedingly  common  and  is  important  as  a 
symptom  associated  with  many  conditions.    Paroxysmal  tachycardia, 

which  we  are  now  to  examine,  is  relatively  rare,  and  is  associated 
with  phenomena  so  distinct  and  definite  that  the  syndrome  deserves 
consideration  as  a  clinical  entity. 

This  group  is  particularly  characterized  by  the  suddenness  of 
the  change  in  the  rate  of  the  heart.  The  acceleration  in  rate  occurs 
as  a  paroxysm  whose  onset  is  abrupt  and  whose  termination  is 
equally  sudden.  The  change  in  rate,  both  of  the  onset  and  off- 
set of  the  attack,  occurs  in  a  period  of  time  less  than  that  occu- 
pied by  one  normal  cardiac  cycle.  The  duration  of  the  paroxysms 
are  extremely  variable.  They  may  last  for  only  a  few  beats  or 
may  continue  for  minutes,  hours  or  days.  The  longest  attack  which 
has  come  under  my  notice  was  continued  for  28  days.  This  varia- 
bility is  the  rule  not  only  comparing  different  cases,  but  also  in 
the  successive  attacks  of  a  single  individual.  The  relative  time 
consumed  by  the  paroxysms  and  the  intervals  of  slow  rate  is  very 
variable,  but  in  nearly  all  instances  the  slow  periods  exceed  the 
paroxysmal  periods  by  a  considerable  margin. 

MECHANISM 

An  analysis  of  the  paroxysms  shows  that  it  is  composed  of  a 
series  of  contractions  having  their  origin  in  some  part  of  the  cardiac 
musculature  other  than  the  sinus  node;  in  other  words,  a  rapid 
succession  of  extrasystoles ;  in  some  point  of  the  heart  wall  ex- 
citability is  raised  to  such  a  point  that  for  a  period  stimuli  are 
set  free  at  an  abnormally  rapid  rate,  and,  in  accordance  with  the 
law  that  the  most  excitable  portion  of  the  heart  sets  the  rate  for 
the  less  excitable  portions,  this  excessively  irritable  point  usurps 
the  function  of  the  pacemaker,  and  for  the  time  the  normal  pace- 
maker, the  sinus  node,  is  buried  in  the  flood  of  stimuli  arising  from 
this  new  point  of  origin.  Usually  all  of  the  contractions  of  a 
given  paroxysm  arise  from  a  single  point  and  spread  over  the  heart 

90 


Paroxysmal  Tachycardia  91 

muscle  by  the  same  path.  This  is  shown  by  the  similarity  of  the 
waves  obtained  in  graphic  records.  For  the  most  part,  the  con- 
tractions arc  rhythmic,  hence  their  rate  is  to  a  degree  a  measure 
of  the  rate  of  stimulus  formation  and  the  excitability  of  the  irri- 
table point. 

During  the  period  of  slowing,  the  sinus  node  regains  its  ascend- 
ency and  sets  the  pace.  Jf  one  studies  carefully  the  periods  of 
slow  rate,  one  will  almost  invariably  discover  isolated  extra 
toles  occurring  more  or  less  frequently.  These  are  usually  of  the 
same  type  as  those  which  go  to  make  up  the  beats  of  the  parox- 
ysm, and  are  often  of  material  assistance  in  determining  the  par- 
ticular point  in  the  heart  in  which  the  extrasystoles  of  the 
paroxysms  have  their  origin.  It  is  conceivable  that  any  portion  of 
the  heart  muscle  may  be  capable,  under  suitable  conditions,  of 
assuming  the  role  of  pacemaker  for  a  limited  period  of  time.  We 
are  certainly  able  to  define  paroxysms  which  have  their  origin  in 
the  wall  of  the  auricle,  in  the  region  of  the  auriculo-ventricular  node 
and  in  the  right  and  left  ventricles.  Most  of  the  paroxysms  have 
an  auricular  origin.  Ventricular  paroxysmal  tachycardias  are  com- 
paratively rare. 

When  the  point  of  origin  is  in  the  auricle,  the  ventricle  usually 
responds  promptly  and  in  the  usual  manner  to  each  auricular  im- 
pulse. At  times,  however,  the  electrocardiographic  records  sug- 
gest that  the  stimulus  has  taken  a  path  through  the  ventricle  wall, 
somewhat  removed  from  the  normal,  or  again  the  exciting  effects 
of  the  frequent  stimuli  may  be  seen  in  a  depression  of  the  bundle 
contractility,  as  evidenced  by  an  abnormally  long  period  between 
the  auricular  and   ventricular  contractions. 

It  has  been  shown  by  Erlanger*  that  stimuli  may  pass  over  the 
conducting  system  of  the  heart  in  a  direction  opposite  to  the  nor- 
mal. We  have  evidence  that  this  occurs  in  paroxysms  of  ven- 
tricular origin,  and  that  the  auricular  contraction  is  a  response  to 
stimuli  reaching  it   from  the  ventricle. 

EXPERIMENTAL   PRODUCTION 

In  a  previous  chapter  it  has  been  pointed  out  that  single  extra- 
systoles  may  be  produced  experimentally  by  applying  mechanical 

*Arch.  Int.  Med.,  1913,  xi,  p.  362. 


92  Paroxysmal  Tachycardia 

or  electrical  stimuli  to  various  portions  of  the  cardiac  musculature. 
If  a  properly  spaced  series  of  such  stimuli  are  applied  to  the  wall 
of  the  heart,  a  tachycardia  will  instantly  result,  composed  of  a 
succession  of  extrasystoles.  During  such  an  artificial  paroxysm, 
the  activity  of  the  normal  pacemaker  is  submerged  by  the  stimuli 
set  free  from  the  new  focus.  When  the  artificial  stimuli  are  with- 
drawn the  tachycardia  terminates  abruptly.  The  normal  pace- 
maker immediately  regains  its  ascendency  and  the  normal  rhythm 
is  resumed.  Such  paroxysms  may  be  induced  by  stimulation  of 
either  the  auricle  or  the  ventricle.  When  the  ventricle  is  thus 
excited,  the  stimuli  are  transmitted  upward  to  the  auricle,  a  direc- 
tion the  reverse  of  the  normal,  and  the  contractions  follow  instead 
of  precede  the  ventricular  contractions.  These  retrograde  stimuli 
pass  the  bundle  of  His  with  less  velocity  than  those  which  pass 
over  the  heart  in  the  normal  direction,  hence  a  part  of  them  may 
be  blocked  and  the  auricle  may  fail  to  respond  to  each  ventricular 
contraction.  Tachycardias  have  been  experimentally  produced  by 
the  administration  of  aconitin  (Cushny),  muscarine  (Rothberger 
and  Winterberg),  by  an  abrupt  increase  of  the  blood  pressure 
(Hering),  and  by  ligature  of  the  coronary  arteries  (Lewis)  ;  a 
production  of  attacks  of  tachycardia  by  ligation  of  the  coronaries 
particularly  elicits  our  interest,  since  it  more  nearly  approximates 
conditions  which  we  may  encounter  clinically.  Lewis*  found  that 
obstruction  of  the  blood  flow  in  the  right  coronary  was  usually, 
and  that  of  the  descending  branch  of  the  left  coronary  was  in- 
variably, followed  by  isolated  ventricular  extrasystoles,  as  the  nu- 
trition of  that  portion  of  the  ventricular  wall  supplied  by  these 
vessels  became  progressively  impaired,  extrasystoles  appeared  at 
shorter  and  shorter  intervals,  until  finally  there  was  established  a 
rapid  series  of  rhythmically  recurring  extrasystoles,  constituting 
a  true  paroxysmal  tachycardia.  Under  these  conditions  the  stimuli 
became  retrograde  and  the  auricular  followed  the  ventricular  con- 
traction. The  extrasystoles  were  rhythmical  and  graphic  records 
showed  that  in  a  given  case  all  the  extrasystoles  had  a  single  point 
of  origin.  In  dogs  rates  between  300  and  420  per  minute  were 
obtained.  The  phenomenon  occurred  both  when  the  vagi  were 
intact  and  when  they  were  sectioned,  showing  that  the  disturbance 
♦Heart,   1909-10,   i,   p.  98. 


I  'aroxysmal  Tachycardia 


93 


TTTTTTTfl     J 


^H 


ffi 


A-V 


\ 


Figure  60 

Diagram  showing  mcclianism  of  auricular  tachycardia.  One  isolated  extrasystolc  is 
indicated  and  a  short  paroxysm  composed  of  a  rhythmic  series  of  similar  extrasystoles. 
The  temporary  pacemaker  is  located  in  the  wall  of  the  auricle.  The  conduction  time 
{A-V  period)   is  lengthened  during  the   paroxysm. 


As 

M 


)  B   5  5 


H 


{((({(i(i 


T  T  T   I   I   I  T  T 


Figure  6i 


Diagram  showing  the  mechanism  of  ventricular  tachycardia.  One  isolated  ventricular 
extrasystole  and  a  short  paroxysm  composed  of  a  rhythmic  series  of  similar  extrasystoles. 
The  temporary  pacemaker  is  located  in  the  ventricular  wall.  During  the  paroxysm  the 
auricle  contracts  in  response  to  "retrograde  stimuli"  passing  upward  from  the  ventricle, 
every  other  impulse  from  the  ventricle  is  blocked. 

The  arrows  indicate  the  points  of  origin  and  the  direction  taken  by  the  stimuli.  Dot- 
ted arrows  indicate  the  time  at  which  the  normal  stimulus  at  the  sinus  node  should  reach 
maturity  if  its  formation  were  not  interrupted  by  the  extrasystole.  The  thickness  of  the 
lines  representing  ventricular  systole  indicate  the  relative  effect  of  the  normal  beat  and 
the  beats  of  the  paroxysm  in  maintaining  an  adequate  circulation.  As  =  auricular  svstole. 
A-V  =  time  of  transition  from  auricle  to  ventricle  or  the  reverse.     \"s  =  ventricular  systole. 


ij4  Paroxysmal  Tachycardia 

had  its  origin  in  the  wall  of  the  heart  and  could  not  be  as- 
cribed to  altered  central  innervation.  When  the  ligature  was 
removed  and  the  circulation  became  re-established,  the  paroxysm 
abruptly  ceased  and  the  sinus  node  resumed  its  function  of  pace- 
maker. 

The  diagrams,  Figures  60  and  61,  indicate  the  mechanism  of  the 
paroxysmal  attacks.  Figure  <>o  represents  a  focus  of  abnormal  irri- 
tability situated  in  the  wall  of  the  auricle.  The  impulses  are  set 
free  so  rapidly  that  the  stimulus  material  forming  at  the  sinus  node 
is  destroyed  before  reaching  maturity.  As  soon,  however,  as  the 
abnormal  irritability  of  the  auricular  wall  is  lost,  the  accumulation 
of  stimulus  material  at  the  sinus  node  continues  for  the  normal 
period  and  thus  the  node  resumes  its  role  of  pacemaker.  Figure 
Ci  represents  an  abnormal  focus  in  the  ventricular  wall,  which,  for 
a  short  period,  becomes  the  pacemaker  of  the  whole  heart.  Here 
the  ventricular  impulses  become  retrograde,  that  is,  they  passed  up- 
ward over  the  A-V  bundle  and  stimulated  the  auricle  from  below. 
These  impulses  are  frequently  blocked,  as  is  indicated  in  the  dia- 
gram, in  which  the  auricle  responds  only  to  every  other  ventricular 
impulse. 

It  might  be  supposed  from  this  review  of  the  mechanism  of  these 
disturbances  that  paroxysmal  tachycardias  would  be  frequent  se- 
quela? of  single  extrasystoles.  This  is  not  the  case.  Isolated  extra- 
systoles  are  extremely  common.  Probably  most  individuals  reach- 
ing the  age  of  50  have  had  extrasystoles  at  one  time  or  another, 
but  attacks  of  true  tachycardia  are  comparatively  rare.  On  the 
other  hand,  it  may  be  said  that  probably  every  true  paroxysm  is 
preceded  by  isolated  extrasystoles. 

PATHOLOGY 

Little  is  known  of  the  histological  changes  which  may  form  the 
anatomical  basis  of  paroxysmal  tachycardia.  In  my  own  series  only 
two  cases  have  had  a  fatal  termination,  and  in  neither  of  these 
was  a  post  mortem  permitted.  In  the  literature  several  autopsies 
have  been  reported  and  these  have  all  shown  more  or  less  ex- 
cessive myocardial  change — sclerosis,  fibrosis,  atrophy,  and  arterial 
degeneration,  particularly  of  the  coronaries.  One  does  not  feel  that 
we  have  as  yet  evidence  of  any  definite  pathological  lesion  which 


Paroxysmal  Tachycardia  95 

is  characteristic.  Experimental  evidence  suggests  that  the  cause 
may  be  found  in  the  intracellular  chemical  change  induced  by  vari- 
ations in  the  blood  supply  in  the  heart,  which  may  or  may  not 
show  degeneration  of  the  myocardium. 

ETIOLOGY 

In  no  one  of  my  scries  of  33  cases  of  paroxysmal  tachycardia 
have  I  been  able  to  obtain  a  history  of  a  similar  condition  in  an 
ancestor  or  in  any  immediate  relative.  My  youngest  case  was  a 
girl  who  had  her  first  attack  when  9  years  of  age;  the  oldest  a 
man  of  69,  whose  paroxysms  had  annoyed  him  for  2  years.  One 
patient,  a  man  of  44,  has  suffered  from  attacks  over  a  period  of 
20  years.  The  distribution  by  decades  of  the  time  of  onset  in 
my  series  is  as  follows: 

Decade Under  10  10-20  20-30  30-40  40-50  50-60  60-70 

Number  of  Cases  . .         1  486653 

Among  the  33  cases  which  I  have  observed,  23  were  males  and  10 
females.  The  following  tabulation  indicates  that  the  syndrome  oc- 
curs about  twice  as  often  in  men  as  in  women. 

Hoffmann*        Lewisf 

Men    6  18 

Women 4  11 


Hart 

Total 

23 

47 

10 

25 

2 


An  analysis  of  my  cases  presents  the  following  factors,  which 
may  have  a  bearing  direct  or  indirect  on  the  condition  of  the  myo- 
cardium. Alcohol  was  used  to  excess  by  4 ;  tobacco  by  2  of  the 
men.  Severe  gastrointestinal  disturbance  had  preceded  the  attacks 
for  several  years  in  3  of  the  women;  nearly  all  had  a  history  of 
one  or  more  of  the  infectious  diseases  of  childhood;  in  one  case 
the  onset  of  tachycardia  followed  6  months  after  a  severe  infec- 
tion of  the  middle  ear ;  in  another  yellow  fever  antedated  the  at- 
tacks by  2  years.  There  had  been  frank  attacks  of  acute  articular 
rheumatism,  followed  by  endocarditis  with  valvular  defects,  in  4 
cases ;  a  syphilitic  infection  was  demonstrable  in  4  cases,  3  of  which 

*Die  Electrocardiographic.  Wiesbaden.   1014. 
tClinical  Disorders  of  the  Heart  Beat,  London,  1913. 


96  Paroxysmal  Tachycardia 

showed  evidence  of  myocardial  damage  other  than  the  attacks  of 
tachycardia.  Several  of  the  scries  had  taken  considerable  doses 
of  digitalis;  in  one  a  physician  whose  arrhythmia  had  been 
wrongly  diagnosed  as  complete  irregularity  and  auricular  fibrilla- 
tion had  taken  very  large  doses,  and  it  seems  to  me  that  this  was 
undoubtedly  an  important  agent  in  increasing  the  irritability  of 
the  heart  muscles.  The  attacks  in  a  young  patient  of  my  series, 
a  hoy  of  ten,  immediately  followed  a  race  in  which  he  par- 
ticipated, at  which  time  the  physician  who  saw  him  found  evidence 
of  acute  dilatation.  A  case  of  mild  Graves'  disease,  in  which  the 
pulse  averaged  100,  has  shown  on  several  occasions  paroxysms 
lasting  only  a  few  minutes  in  which  the  rate  was  between  160  and 
I/O.  Valvular  defects  were  present  in  1  _'  of  my  patients;  the 
mitral  valve  was  involved  in  10,  of  which  4  were  cases  of  well- 
marked  stenosis;  two  patients  had  aortic  insufficiency  and  one 
had  defects  of  both  the  aortic  and  mitral  valves;  15  cases  showed 
various  decrees  of  cardiac  enlargement.  In  many  cases  the  irri- 
tability of  the  heart  muscle  seems  to  require  a  very  small  excit- 
ing factor  to  induce  an  attack.  The  patient  will  usually  ascribe 
the  onset  to  flatulence,  some  emotional  disturbance  or  unusual 
physical  exertion ;  any  one  of  these  is  probably  an  efficient  cause 
to  call  forth  an  attack  in  a  myocardium  suitably  damaged. 

SYMPTOMS 

The  symptoms  associated  with  paroxysmal  tachycardia  arc  of 
great  variety,  and  show  great  differences  from  individual  to  indi- 
vidual. This  is  doubtless  in  a  large  measure  due  to  the  extent  of 
damage  present  in  the  myocardium  and  the  ability  of  the  heart 
to  meet  the  tax  thus  exacted.  The  patient  is  practically  always 
conscious  of  the  abrupt  onset  and  termination  of  the  attacks.  They 
usually  describe  the  attacks  as  beginning  with  one  or  two  "thumps" 
or  "throbs"  in  the  precordial  region,  followed  by  a  sensation  of  flut- 
tering in  the  chest,  which  is  terminated  by  another  "thump"  or 
"flop,"  and  the  attack  is  over.  The  amount  of  anxiety  is  always 
greater  in  the  early  attacks;  as  the  patient  becomes  more  or  less 
accustomed  to  the  paroxysm  he  is  less  alarmed,  and  a  momentary 
pause  in  his  activities  may  be  the  only  evidence  to  show  that  he 
knows   the  attack   is   on.      This  absence  of  alarm   I   have   noticed 


Taroxysmal  Tachycardia  (ji 

particularly  in  young  adults  who  have  had  attacks  for  a  number 
of  years,  but  whose  hearts  show  no  anatomical  abnormality  and 
functional  disturbance  characterized  only  by  the  attacks  of  extra- 
systoles  at  more  or  less  infrequent  intervals. 

One  of  my  patients,  whose  attacks  have  continued  for  several 
days,  was  quite  unconcerned  even  when  his  heart  was  beating  at 
170.  He  rarely  voluntarily  assumed  a  recumbent  position  on  ac- 
count of  the  attacks  and  it  was  difficult  to  convince  him  that  rest 
at  these  times  was  important. 

In  those  who  have  an  associated  valvular  lesion,  and  in  those 
with  evidence  of  marked  arterial  changes,  a  greater  discomfort  and 
attendant  anxiety  are  closely  associated  with  the  symptoms  re- 
ferable to  the  cardiac  insufficiency  which  is  induced  by,  or  the 
precordial  pain  which  accompanies,  the  attack. 

At  the  onset  patients  often  complain  of  palpitation  in  the  chest 
and  a  swelling  and  pulsation  of  the  vessels  of  the  neck.  Often 
they  have  eructations  of  gas,  nausea  and  vomiting.  There  may 
be  a  "gone,"  sinking  feeling,  and,  if  the  attack  is  prolonged,  sweat- 
ing, coldness,  great  lassitude  and  an  intolerable  feeling  of  weak- 
ness. They  may  have  a  sensation  of  palpitation  or  of  bounding  in 
the  chest,  shortness  of  breath  or  a  sensation  of  suffocation.  In  one 
case  under  my  observation  attacks  were  invariably  accompanied  by 
a  watery  diarrhoea ;  in  another  by  frequent  micturition. 

In  the  prolonged  attacks,  increase  of  the  cardiac  dulness  to  the 
left  can  sometimes  be  made  out  and  the  symptoms  of  circulatory  em- 
barrassment terminate  the  picture.  The  veins  are  not  properly 
emptied,  but  are  engorged,  and  there  is  pronounced  cyanosis.  The 
liver  may  be  increased  in  size  and  become  tender  to  palpation.  There 
may  be  edema  of  the  extremities ;  there  may  be  cough  with  profuse 
thin,  or  blood-streaked,  expectoration,  with  the  physical  signs  of 
pulmonary  congestion. 

The  paroxysms  are  often  attended  with  headache  and  dizziness, 
more  rarely  with  momentary  or  prolonged  periods  of  unconscious- 
ness, which  may  be  explained  on  the  basis  of  cerebral  anemia.  Pain 
is  sometimes  prominent.  A  feeling  of  oppression  and  of  constric- 
tion of  the  chest  accompanies  the  attacks  in  nearly  all  patients  to 
a  greater  or  less  degree.  The  pain  is  usually  precordial,  and  is 
sometimes  sharp,  suggesting  a  real  angina,  and  may  radiate  into 


98  Paroxysmal  Tachycardia 

the  arms  and  back:  sometimes  one  can  detect  areas  of  hyperesthesia 
over  the  chest  and  arms,  following  the  distribution  of  one  or  more 

of  the  upper  thoracic  and  lower  cervical  nerves.  A  tew  patients 
complain  of  numbness  and  tingling  of  the  extremities. 

A  progressive  cardiac  insufficiency  may  terminate  in  general 
anasarca,  pulmonary  edema,  collapse  and  occasionally  death.  As  a 
rule,  however,  the  signs  of  cardiac  insufficiency  are  very  moderate, 
and  even  when  present  to  an  extreme  degree  clear  up  with  great 
rapidity,  following  the  abrupt  ending  of  the  rapid  heart  action.  The 
absence  of  alarm,  the  facial  change  of  expression  from  one  of 
anxiety  to  complete  calm ;  the  abrupt  change  from  dyspnea  to  quiet 
breathing;  the  sudden  cessation  of  pain;  the  subsidence  of  en- 
gorged veins  of  the  neck  coincident  with  the  termination  of  the 
paroxysm  present  some  of  the  most  remarkable  and  agreeable  clin- 
ical phenomena  with  which  we  are  familiar. 

The  signs  of  pulmonary  congestion  and  edema  of  the  extremi- 
ties may  require  a  period  of  days  for  their  subsidence,  the  rapidity 
depending  to  a  considerable  degree  on  the  functional  efficiency  of 
the  heart  when  it  has  resumed  its  normal  rate. 

As  illustrating  the  character  of  severe  attacks  terminating  fatally, 
one  case  which  I  had  the  opportunity  to  observe  closely  for  a  period 
of  months,  may  be  described. 

A  man,  55  years  of  age,  who  had  a  leutic  infection  20  years 
earlier,  had  a  heart  moderately  enlarged  to  the  left  and  a  faint 
systolic  murmur  at  the  apex.  Between  the  attacks  his  pulse  was 
about  70  with  many  extrasystoles.  At  all  times  there  was  evi- 
dence of  a  moderate  degree  of  cardiac  insufficiency.  A  descrip- 
tion of  the  attacks,  obtained  from  the  patient,  was  as  follows: 

"The  exact  cause  of  these  attacks  of  syncope  and  tachycardia, 
which  come  as  often  as  twenty  times  in  one  day  and  have  been  ab- 
sent as  long  as  26  days,  cannot  be  determined.  Many  times  he 
has  been  wakened  from  his  sleep  by  dizziness  to  become  uncon- 
scious and  have  a  typical  attack.  Again,  a  slight  exertion,  as  walk- 
ing, going  up  stairs  or  straining  to  pass  water,  may  be  followed  by 
an  attack,  but  these  same  exertions,  or  even  more  severe  ones  at 
another  time,  may  have  no  harmful  effect.  The  attack  comes  on 
suddenly  with  dizziness,  grayness  before  the  eyes  and  a  buzzing  in 
the  head  like  an  organ.    There  are  no  premonitory  symptoms,    Un- 


Paroxysmal  Tai  [iycardia 


99 


iK'j'ar 


Brachial 


3.2  second 


Figure  62 

Normal.      Rate   82.      Respiratory   rate    24.      For   paroxysm   of   auricular    tachycardia   in 
the    same    individual   see   Figure    63. 


fugular 


Brachial 


second 


Figure  63 


Auricular  tachycardia.  Rate  182.  Respiratory  rate  30.  For  record  of  the  same  case 
Between  attacks  see  Figure  62.  Compare  in  the  two  records  the  volumes  of  the  arterial 
and   venous   pulses.     The   jugular   records   are   quite   different   in   form,    the   large  wave   of 


ioo  Paroxysmal  Tachycardia 

consciousness  follows  rapidly,  and  when  he  comes  to  his  heart  is 
beating  very  rapidly,  200  to  250  to  the  minute.  There  is  a  chok- 
ing sensation,  as  if  a  hall  were  in  the  throat,  and  he  is  shaking  all 
over.  There  is  never  any  pain  over  the  heart  or  down  the  arm. 
At  times  he  has  been  struck  down  as  if  by  electricity  without  warn- 
ing, again  lie  has  simply  had  dizziness  and  grayness,  without  losing 
consciousness.  The  tachycardia  lasts  a  varying  length  of  time, 
sometimes  for  only  ten  minutes,  at  other  times  all  day.  During  its 
continuance  he  has  great  gastric  disturbance,  with  frequent  vomit- 
ing. He  cannot  forecast  the  end  of  the  attacks  until  it  is  at  an 
end.  Then,  at  times,  a  violent  regular  beating  of  the  heart  is  suc- 
ceeded by  two  or  three  irregular  beats,  as  if  something  shook  the 
heart,  and  this  is  immediately  followed  by  two  or  three  tremendous 
throbs  of  the  heart  with  each  of  which  there  is  a  feeling  as  if 
fresh  air  were  forced  into  his  throat  and  head  and  the  attack  stops 
suddenly  as  it  began." 

His  paroxysms  of  tachycardia  continued  for  5  years,  becoming 
gradually  more  frequent,  and  he  finally  died  during  an  attack. 

IDENTIFICATION 

The  conditions  other  than  paroxysmal  tachycardia  which  afford 
a  heart  rate  of  over  160  are  extremely  rare.  During  the  paroxysm 
the  pulse  is  exceedingly  small,  often  irregular  in  force  and  fre- 
quently cannot  be  detected  at  the  wrist.  Under  these  conditions 
our  examination  should  at  once  be  directed  to  the  precordial  region. 
The  apex  beat  may  be  imperceptible  to  the  touch  or,  when  palpable, 
may  give  the  impression  of  complete  irregularity.  The  heart  sounds 
may  be  indistinct  and  have  a  fetal  character;  often  they  are  sharp 
and  distinct ;  as  a  rule,  they  are  perfectly  rhythmic,  but  so  rapid 
that  the  rate  can  be  only  approximately  estimated ;  this  is  best  ac- 
complished by  counting  short  (5  seconds)  periods.  If  one  is  for- 
tunate enough  to  be  making  observations  at  the  beginning  or  at 
the  termination  of  the  attack,  the  change  in  rate  is  readily  detected. 
The  transitions  are  usually  accompanied  by  one  or  two  large  forcible 
heats,  with  loud  sounds  and  unusually  large  pulse  waves.  The 
change  in  rate  is  quite  abrupt.  In  the  absence  of  such  an  observa- 
tion the  patient  will  frequently  establish  the  diagnosis  by  his  de- 
scription of  the  sudden  onset  and  termination  of  the  attacks.    Valvu- 


Paroxysmal  Taciiyi  ardia 


ioi 


■ 


I ! 


WW  0.2  second 


Figure  64 

Rate  72.  Between  attacks  same  individual  as  Figure  65.  At  X  is  shown  an  extrasystole 
with  an  incomplete  compensatory  pause.  Note  the  a  wave  is  large  and  the  a-c  interval  is 
of  normal  length. 


Jugular 


Brachial 


0.2  second 


Figure  65 

Auricular  tachycardia  rate  174.  For  slnw  rate  see  Figure  64.  The  large  venous  waves 
are  the  result  of  the  simultaneous  contraction  of  the  auricle  and  the  ventricle.  Each  one 
of  these  waves  belongs  to  two  cycles.  They  are  composed  of  a  c  wave  of  a  cycle  just  com- 
pleted and  an  o  wave  of  a  cycle  just  beginning.     The  a-c"  interval  is  abnormally  long. 


ioj  Paroxysmal  Tachycardia 

lar  murmurs,  if  present  during  the  slow  rate,  sometimes  cannot  be 
detected  during  the  paroxysm.  In  some  rases  a  heart  without  mur- 
murs during  the  slow  period  will  develop  a  loud  systolic  murmur 
during  the  paroxysms. 

During  the  slow  periods  extrasystoles  followed  by  pauses,  more 
or  less  fully  compensatory,  can  usually  be  detected;  sometimes  they 
are  very  frequent,  more  often  only  occasional.  Single  extrasys- 
toles are  quite  common  between  paroxysms  which  are  of  short 
duration  and  which    follow   one  another  at  brief  intervals. 

During  the  paroxysms  the  veins  of  the  neck  are  prominent,  dis- 
tended, hard  and  pulsate  with  great  rapidity.  ( )ften  two  pulsations 
of  the  jugular  may  be  seen  to  correspond  to  each  systole  of  the 
heart. 

In  most  instances  the  attacks  are  not  affected  by  the  position  as- 
sumed by  the  patient  and  continue  whether  he  sits  up  or  lies  down 
without  change  in  rate. 

When  seen  only  between  the  attacks  the  diagnosis  rests  largely 
on  the  history,  but  the  patient's  description  of  the  attacks  is  usually 
so  clear  that  there  is  little  difficulty  in  classifying  the  abnormal 
activity. 

The  cases  which  present  the  most  obscure  diagnostic  problems  are 
those  with  very  frequent  short  paroxysms  separated  by  equally 
short  periods  of  slow  rate  broken  by  frequently  occurring  extra- 
systoles.  These  are  often  wrongly  classified  as  complete  irregu- 
larity due  to  auricular  fibrillation.  They  may  usually  be  assigned 
to  their  correct  category  by  means  of  a  careful  and  prolonged  study 
of  the  ordinary  physical  signs.  Their  status  may  be  absolutely 
settled  by  graphic  records. 

The  polygram  brings  out  clearly  some  features  of  the  paroxysms 
which  are  observed  with  great  difficulty  by  the  ordinary  means  of 
eliciting  physical  signs. 

In  Figures  62  and  63  are  shown  brachial  and  jugular  tracings 
taken  from  a  woman  35  years  of  age.  Figure  62  shows  the  usual 
condition  of  her  pulse;  the  rate  is  82;  the  arterial  pulse  is  of  good 
size  and  well  sustained;  the  jugular  pulse  shows  a  normal  sequence 
of  waves  a,  c  and  v ;  the  a-c  interval  is  normal  (less  than  0.2  second). 
Figure  63  is  a  record  taken  during  hCr  second  paroxysm,  which 
lasted  2  days  without  interruption.     At  the  time  the  tracing  was 


104  Paroxysmal  Tachycardia 

secured  the  attack  has  been  under  way  for  24  hour?.  The  heart 
at  this  time  was  beating  rhythmically  at  a  rate  of  182  per  minute. 
The  small  volume  of  the  brachial  pulse  is  in  great  contrast  to  that 
ot"  the  slow  periods.  The  venous  curve  shows,  in  place  of  the  well- 
defined  waves  of  the  slow  heart  rati',  one  large  wave  and  one  small 
notch  to  each  cycle.  The  interpretation  is  that  the  auricle  and  the 
ventricle  are  contracting  simultaneously,  so  that  the  veins  are  un- 
able to  empty  into  the  right  auricle  in  the  normal  manner,  ddie 
large  jugular  waves,  much  greater  than  the  jugular  \\a\es  of  the 
normal  period,  are  due  to  a  summation  of  the  a  and  c  waves.  It 
will  also  he  seen  that  during  the  paroxysm  the  a-c  interval  is  con- 
siderably prolonged  (over  0.3  second),  indicating  that  there  is  a 
delay  in  the  conduction  of  the  stimulus  from  the  auricle  to  the 
ventricle.  This  is  not  an  uncommon  feature  in  tachycardias,  the 
excessive  functional  demand  on  the  slender  A-l'  bundle  leading  to 
its  partial  exhaustion. 

In  these  two  figures  the  respiratory  curve  is  brought  out  in  the 
venous  tracing.  That  in  this  case  the  dyspnea  was  not  very  marked 
is  evidenced  by  the  facts  that  the  breathing  was  24  during  the 
slow  rate  and  only  30  during  the  attack,  and  that  the  excursion  is 
not  very  much  greater  during  the  paroxysm. 

Tracings  from  another  case  of  auricular  tachycardia  arc  shown 
in  Figures  (»4  and  65.  As  in  the  preceding  case,  the  contrasts  be- 
tween the  cardiac  rates  (72  and  174)  and  the  arterial  pulse  volumes 
of  the  two  periods  are  shown  in  the  brachial  tracings.  During  the 
paroxysm  (  Figure  65)  only  one  large  wave  appears  in  the  jugular 
to  each  cardiac  cycle. 

The  slow  period  I  Figure  64)  is  interrupted  at  one  point  (  .V  1  by 
an  extrasystole  with  an  incomplete  compensatory  pause,  hence  we 
may  conclude  that  it  probably  had  its  origin  in  the  auricular  wall. 
It  is  a  series  of  such  extrasystoles  which  constitute  the  paroxysm. 

Figure  66  was  taken  from  a  man  of  36  during  a  prolonged  parox- 
ysm. The  ventricular  rate  is  158  and  is  perfectly  rhythmic.  The 
jugular  tracing  shows  the  great  venous  congestion  and  the  very 
large  waves  which  are  due  to  simultaneous  contractions  of  auricle 
and  ventricle;  conduction  is  delayed.  The  exact  point  in  the  auricle 
which  has  become  the  temporary  pacemaker  for  the  whole  heart 
cannot    he    definitely    settled     from    the    polvgraphic    record.      The 


Paroxysmal    I  achycardia 


!<>■■ 


T 


ift^Aj*^^ 


■_f — ■    ,.„,,„■ 

Normal.      Rate  80 

Figure  68 

Same  case  as  Figure  69. 

Lead   II. 

„-Tvr^.inyf  n  '"P1.  ■  i 

,r.  -  r  iTf 


Figure  60 

Taken  during  a  paroxysm,  rate  167.  Lead  II.  Same  patient  as  Figure  68.  Xote 
inversion  of  P,  which  notches  the  summit  of  T,  Auricular  tachycardia.  The  pacemaker 
of  the  heart  is  in  the  lower  part  of  the  auricle. 


nx>  Paroxysmal  Tachycardia 

respiratory  curve  upon  which  the  large  jugular  wave?  .ire  super- 
imposed  show  that,  in  spite  of  the  prolonged  attack,  the  breathing 

is  not  greatly  accelerated;  at  this  time  it  was  22  to  the  minute,  but 
quite  irregular. 

A  rare  tracing  from  a  case  of  ventricular  tachycardia  is  repro- 
duced in  Figure  67.  The  brachial  shows  at  A  the  usual  rate  for 
this  patient  between  attacks   (92  per  minute  1.     At   X  isolated  cxtra- 

systoles,  each  with  a  complete  compensatory  pause,  occur;  the 
premature  beats  are  so  weak  that  they  make  practically  no  impres- 
sion on  the  brachial  pressure.  At  B  are  shown  two  short  paroxysms 
of  tachycardia,  indicating  the  manner  of  the  abrupt  onset  and  termi- 
nation of  the  attacks.  The  a-C  interval  of  the  "normal"  rhythm  of 
this  patient  was  always  longer  than  that  of  a  normal  heart,  meas- 
uring nearly  0.3   second. 

During  the  paroxysm  the  auricle  contracted  in  response  to  the 
"retrograde  stimulus"  from  the  ventricle;  this  cannot  be  conclusively 
made  out  in  the  polygram,  but  is  substantiated  by  electrocardio- 
graphic records  (see  Figure  80).  The  irregularity  of  this  pulse  is 
so  extreme  that  it  might  easily  have  been  mistaken  for  a  case  of 
"complete  irregularity"  and  auricular  fibrillation,  had  no  graphic 
records  been  secured. 

The  electrocardiogram  gives  us  information  in  regard  to  parox- 
ysmal tachycardia  which  we  can  obtain  by  no  other  method. 
Through  this  agency  we  have  discovered  the  real  mechanism  of  the 
attacks.  The  knowledge  acquired  in  this  way  tends  to  emphasize 
the  importance  of  the  muscle  cell  changes  and  to  minimize  the  role 
played  by  the  extra  cardial  nerves  in  inducing  this  change  in  cardiac 
activity.  These  graphic  records  convince  us  that  a  new  point  in 
the  heart  wall  has  become  the  temporary  pacemaker  of  the  heart. 
The  proof  is  most  clearly  demonstrated,  if  we  study  the  records  of 
such  a  case  as  is  shown  in  Figure  Ho,  where  the  evidence  is  com- 
plete in  a  single  curve.  This  is  from  a  case  of  ventricular  parox- 
ysmal tachycardia,  a  condition  ol  extreme  rarity,  hence  it  will  be 
bitter  to  first  direct  our  attention  to  the  more  common  forms, 
namely,  tachycardias  of  auricular  origin. 

Such  a  case  is  illustrated  in  Figure  69,  which  was  taken  during 
a  paroxysm  in  which  the  heart  rate  was  \()j.  Figure  68  was  se- 
cured from  the  same  patient  a  few  hours  after  the  cessation  of  the 


Paroxysmal  Tachycardia 


107 


^W^JWtaJftvJtaJ^ 


Figure  70 

Same  patient  as  Figure  71.     Rate  76  between  attacks.     Taken  by  lead  II.     P  is  slightly 
notched,   otherwise  the  curve  is   normal. 


Figure  71 

Auricular  paroxysm,  rate  174,  lead  II.     From  same  individual  as  Figure  70.     The  small 
P  wave  is  submerged  in  the  large  T  wave. 


io8  Paroxysmal  Tachycardia 

attack.  This  record  shows  a  perfectly  normal  curve  for  a  heart 
with  a  rate  of  80.  Both  records  were  taken  by  lead  II  (right  arm 
and  left  foot).  If  we  >h<>ukl  superimpose  the  ventricular  portion 
(beginning  of  R  to  the  end  of  /  >  of  the  cycles  shown  in  Figure  <>X 
on  one  of  the  cycles  of  Figure  <»>.  we  would  find  thai  they  corre- 
spond in  every  particular,  except  that  the  summit  of  the  T  wave 
shows  constantly  a  deep  notch.  If  we  compare  the  records  further, 
we  note  that  in  Figure  69  then'  is  no  wave  which  corresponds  to 
the  well-marked  P  wave  of  Figure  68.  Careful  measurement  shows 
that  the  notch  in  the  T  wave  (  Figure  '>'))  Occurs  at  exactly  the  time 
at  which  a  /'  wave  of  the  normal  rhythm  should  precede  the  R 
wave,  hence  we  conclude  that  the  positive  P  wave  of  the  normal 
rhythm  is  replaced  by  a  negative  wave  notching  the  T  wave  of 
the  paroxysm. 

In  studying  the  auricular  extrasystole,  it  was  shown  that  when 
tiie  premature  heat  started  from  a  point  in  the  auricle  at  some 
distance  from  the  sinus  node,  the  P  wave  of  the  electrocardiogram 
was  distorted  in  form,  or  even  completely  reversed  in  direction, 
hence  in  the  records  under  consideration  we  are  led  to  conclude 
that  the  paroxysm  shown  in  Figure  69  is  composed  of  a  series  ol 
extrasystoles  having  their  origin  at  a  point  in  the  auricular  wall 
considerably   removed   from  the  site  of  the  normal   pacemaker. 

Figure  70,  taken  by  lead  II,  shows  a  normal  electrocardiogram, 
except  for  a  slight  notching  of  the  P  wave.  Figure  71  was  taken 
from  the  same  patient  during  an  attack  which  lasted  for  one  hour, 
during  which  the  heart  rate  was  174.  Here  the  ventricular  por- 
tions of  the  two  records  are  almost  identical,  except  that  the  waves 
of  the  paroxysm  are  a  trifle  smaller  than  those  of  the  slow  rate. 
During  the  paroxysm  no  I'  wave  can  he  definitely  located  ;  in  this 
case  it  was  probably  so  small  that  it  caused  no  distortion  of  the 
relatively  large   T  wave. 

F.lectrocardiograms  of  another  case  of  auricular  paroxysmal 
tachycardia  are  shown  in  Figures  72  and  73;  both  records  were 
taken  by  had   111    (left  arm  and  left  leg). 

When  Figure  ~2  was  taken  the  heart  rate  was  j~>  per  minute.  This 
record  shows  several  abnormal  features;  the  P  wave  is  slightly 
notched  and  R  is  directed  downward  (the  latter  feature  is  quite 
usual  in  hypertrophy  of  the  left  ventricle),  T  is  also  directed  down- 


Paroxysmal  Tachy<  ardia 


109 


p — — — rgf^;1 '. — - — • -W- 

P  P 


Figure  72 

SI  >w   period,  same    case   as    L'"igure   73.      Rate   75.      Lead   III.      P   is   11  itched,    /<"   and    T 

liave   a    downward   direction. 


Figure  73 

Auricular  tachycardia,  rate   16S.     Lead   III.     Same  patient  as  Figure   72.     Ventricular 
complex  increased  in  size.     T  has  become  a  positive  wave.     P  is  superimposed  on  7\ 


no  Paroxysmal  Tachycardia 

\v;ml.  During  the  paroxysm  (Figure  73)  the  rate  is  168.  7v  is  still 
directed  downward  and  is  increased  in  amplitude,  suggesting  a  dila- 
tation oi  the  left  ventricle.  The  slow  wave  between  the  R  waves 
is  an  algebraic  sum  oi  the  waves  P  and  T  of  the  new  rhythm. 

The  next  case,  illustrated  in  Figures  74  and  j^.  shows  some  in- 
teresting features,  during  the  slow  period  (rate  76  per  minute) 
the  /'  wave  is  unusually  broad.  R  is  slightly  notched  and  the 
rhythm  is  broken  by  an  extrasystole,  which  is  plainly  of  ventricu- 
lar origin.  The  paroxysm  ^rate  188)  is  composed  of  A'  waves  fol- 
lowed by  a  depression,  which  in  all  probability  are  reversed  P  waves, 
having  their  point  of  origin  in  the  lower  part  of  the  auricle,  pos- 
sibly near  the  A-V  node.  The  P-R  interval  is  prolonged,  measuring 
Over  o.J  second,  exhibiting  the  delay  in  conduction  which  is  not 
an  uncommon  feature  of  these  cases.  In  this  instance  the  com- 
plexes of  the  paroxysm  probably  represent  extrasystoles  of  auricu- 
lar origin  and  do  not  conform  to  the  type  of  the  isolated  extrasys- 
tole which  interrupts  the  slow  rhythm    (Figure  74). 

Figures  76,  jy  and  jS  depict  the  mode  of  transition  from  the 
slow  to  the  rapid  and  from  the  rapid  to  the  slow  rate  in  different 
cases. 

The  onset  of  a  paroxysm  can  be  seen  in  Figure  76  and  the  dis- 
location of  the  pacemaker  from  the  sinus  node  to  a  point  low 
down  in  the  auricle  is  indicated  by  the  change  in  forms  of  the  P 
Wave  from  a  positive  to  a  negative  deflection.  In  the  first  cycle 
of  the  paroxysm  the  reversed  P  wave  falls  at  the  apex  of  the  T 
wave,  but  subsequently  notches  the  earlier  portions  of  this  part 
of  the  ventricular  complex. 

The  offset  of  a  paroxysm  is  shown  in  Figure  yj.  The  bizarre 
complexes  which  intervene  between  the  paroxysm  and  the  slow 
rhythm  probably  represent  extrasystoles  of  unusual  types,  and 
are  doubtless  the  kind  of  cardiac  activity  which  give  the  patient 
the  subjective  sensation  of  "throbs"  or  "thumps"  at  the  time  of  the 
transition. 

Another  transition  from  a  heart  beat  of  160  to  one  of  70  is 
shown  in  Figure  78.  The  curve  is  somewhat  distorted  by  the  move- 
ments of  the  patient  produced  by  the  sensations  experienced  at  the 
time  of  the  termination  of  his  attack. 

The  most  convincing  evidence  of  the  nature  of  the  mechanism 


Paroxysmal  Tachycardia 


Figure  74 

Rate   of   76   interrupted  by  a  ventricular   extrasystole.      Same   individual   as    Fij/ure   y- 
Lead  11. 


n    a    ** 


3 — ' 


Figure  75 

Paroxysm  of  tachycardia,  rate  1R8.  Lead  II.  From  same  case  as  Figure  74.  Note 
reversal  of  P  wave  and  prolonged  P-R  interval.  Abnormal  pacemaker  probably  situated 
near  the  A-V  node. 


ii2  Paroxysmal  Tachycardia 

in  paroxysmal  tachycardia  is  brought  to  view  when  we  are  fortu- 
nate enough  to  secure  in  a  single  record  periods  of  slow  rates  in- 
terrupted by  single  extrasystoles,  continued  into  periods  of  tachy- 
cardia.    Such  records  are  shown  in   Figures  79  and  So. 

A  short  paroxysm  of  tachycardia  (rate  lUS),  changing  to  a  slow 
rate  (86)  broken  by  extrasystoles,  is  shown  in  Figure  79.  The 
patient,  from  whom  this  curve  was  taken,  was  a  physician,  65  years 
of  age,  in  whom  the  diagnosis  of  "complete  irregularity,"  due  to 
auricular  fibrillation,  had  been  repeatedly  made.  The  correct  diag- 
nosis was  hardly  possible  until  electrocardiographic  records  were 
secured.  The  slow  rate  is  interrupted  by  auricular  extrasystoles 
(A',)  and  another  type  of  extrasystole  (A\.)  which  has  Its  origin 
in  the  ventricular  wall.  The  auricular  premature  beats  have  their 
origin  high  up  in  the  auricle,  since  the  P  wave  of  the  extrasystole 
is  a  positive  wave,  as  is  shown  by  the  waves  which  are  clearly 
the  sum  of  T  and  P.  The  paroxysm  is  composed  of  both  kinds 
of  extrasystoles,  hut  the  auricular  type  predominates,  which  is 
also  the  case  in  the  period  of  slower  cardiac  activity 

The  electrocardiogram  of  a  case  of  ventricular  tachycardia*  is 
shown  in  Figure  80.  Tachycardias  of  this  type  are  extremely  un- 
usual. The  bizarre  forms  of  the  complexes  of  his  slow  rate  (80) 
are  seen  in  the  short  diastolic  (T-P)  interval,  the  broad  P  wave, 
the  long  P-R  interval  and  the  unusual  form  of  the  R  waves.  These 
features  alone  suggest  serious  myocardial  damage.  From  time  to 
time  there  appear  isolated  ventricular  extrasystoles  (A').  The 
paroxysm  (rate  200)  is  composed  of  complexes  similar  in  form 
to  those  of  the  isolated  extrasystoles.  Between  the  large  waves 
of  the  paroxysmal  period  are  seen  small  waves  (P)  which  occur 
with  every  other  cycle.  These  undoubtedly  represent  auricular  con- 
tractions due  to  retrograde  stimuli  arising  in  the  ventricle.  It  ap- 
pears that  every  other  impulse  from  the  ventricle  is  blocked.  This 
record  conforms  in  many  particulars  to  the  curves  obtained  experi- 
mentally after  tying  one  of  the  coronary  arteries,  hence  a  tentative 
diagnosis  may  be  made  of  partial  coronary  obstruction.  The  pa- 
tient is  still  alive  (3  years  after  the  record  was  taken),  hence  the 
diagnosis  has  not  been  verified. 

*A  complete  record  of  this  case  will  be  found  in  Heart,  1012,  iv,  p,  128. 


Paroxysmal  Tachycardia 


"3 


^^S^^-^T. 


W— 


w-  W- 


Figure  76 

Transition    from    slow    rate   to    paroxysm.      Note    dislocation    of   pacemaker   to    a    point 
low  down  in  the  auricle  as  evidenced  by  the  abrupt  change  in  the  direction  of  the  /' 
The  ventricular  complex  is   unchanged  except  as   its  contour   is  broken  by  the  rever 
wave.     Compare  Figure  69. 


J 

K         •*        ^         0  J 

L- _ — , — _ , , , , 

Figure  77 

Abrupt  termination  of  a  paroxysm.     Transition   distorted  by  extrasystoles   of  ventricu- 
lar origin.      Pacemaker  of  paroxysm  located   near  the  A-V  node.     Compare   Figure    -5. 


FT 


J„1_T_T 


Vi/^glV^ 


T 


Figure  78 

Auricular  tachycardia,  rate   160.     Transition  to  rate  of  70.     Origin  low  down   in  the 
auricle. 


114  Paroxysmal  Tachycardia 

CLINICAL  SioNiruwNii-:  and  prognosis 

There  is  little  doubt  that  every  subject  of  paroxysmal  tachycardia 
has  a  defect  of  the  myocardium  that  must  be  seriously  considered. 
The  prognosis  is  most  difficult.  Some  patients  over  a  period  of 
many  years  have  attacks  which  incommode  them  but  little  and  the 
attacks  become  less  severe,  less  alarming,  and  in  some  instances 
disappear  altogether.  Some  have  only  a  few  attacks  before  the 
fatal  termination. 

1  have  never  seen  a  case  that  was  fatal  until  a  number  of  at- 
tacks had  occurred,  nor  have  I  found  such  a  case  reported  in  the 
literature. 

The  condition  of  the  heart  in  the  intervals  between  attacks  is 
important  as  an  aid  in  determining  the  seriousness  in  the  individual 
case.  If  at  these  times  the  heart  shows  no  abnormality  other  than 
occasional  extrasystoles,  one  can  be  reasonably  sure  that  there  is 
no  imminent  danger.  If,  however,  marked  valvular  defects  are 
present,  if  there  is  evidence  of  an  old  inflammation  of  the  peri- 
cardium, if  there  is  a  general  arteriosclerosis,  if  extrasystoles  con- 
stantly occur  at  very  frequent  intervals,  and  if  the  heart  is  embar- 
rassed in  maintaining  an  adequate  circulation  in  the  periods  of 
slow  rate,  the  paroxysms  will  rightly  be  viewed  with  much  appre- 
hension. The  paroxysm  is  very  exhausting  to  the  heart.  If  the 
myocardial  damage  is  made  evident  by  the  attacks  only,  the  heart 
will  probably  successfully  carry  this  stress;  if,  however,  other  evi- 
dences of  myocardial  damage  exist,  the  strain  of  the  paroxysm  is 
a  far  more  serious  matter.  The  patients  who  do  particularly  well 
are  young  subjects  with  no  evidence  of  cardiac  abnormality  be- 
tween attacks.  Middle-aged  and  elderly  individuals  sooner  or  later 
invariably  develop  other  evidences  of  myocardial  insufficiency  and, 
while  they  may  have  many  and  frequent  attacks  of  tachycardia 
without  serious  manifestations,  the  ultimate  outlook  is  less 
favorable. 

The  frequency  and  duration  of  the  individual  attacks  do  not 
seem  to  be  very  important  factors  in  determining  the  prognosis. 
Much  more  important  is  the  severity  of  the  attacks  as  estimated 
by  the  degree  of  circulatory  embarrassment,  cardiac  dilatation,  the 
congestion  of  lungs  and  liver  and  edema  of  the  extremities.     At- 


u6  Paroxysmal  Tachycardia 

tacks  associated  with  unconsciousness  should  be  viewed  with  gravity. 
With  a  history  of  a  moderate  number  of  attacks  over  a  number 

of  years  in  a  young  adult,  with  intervening  periods  of  normal  heart 
action,  one  may  usually  give  a  good  prognosis.  When  the  patient 
is  moie  advanced  in  years  and  has  paroxysms  of  increasing  fre- 
quency and  severity,  and  intermediate  periods  characterized  by  signs 
of  cardiac  insufficiency,  the  outcome  of  any  particular  attack  is 
doubtful,  the  prognosis  for  the  future  is  not  good. 

There  is  another  rare  form  of  paroxysmal  tachycardia  in  which 
the  attack  consists  in  a  short  period  of  auricular  fibrillation.  This 
will  be  discussed  in  the  chapter  on  auricular  fibrillation. 


CHAPTER  X 

Auricular  Flutter 

Closely  allied  to  "auricular  paroxysmal  tachycardia,"  discussed 
in  the  last  chapter,  is  an  abnormal  functional  activity  of  the  hearl 
usually  designated  as  auricular  flatter*  The  terms  "auricular 
tachycardia"  (Robinson),  "auricular  tachyrhythmia"  (Hoffmann;, 
and  "auricular  tachysystole"  (Rihl)  have  also  been  applied  to  this 
condition. 

The  chief  distinguishing  feature  of  this  group  is  the  rapid,  rhyth- 
mic, coordinated  systoles  of  the  auricle,  the  contractions  usually 
occurring  at  a  rate  between  250  and  300  per  minute.  The  auricular 
rate  is  so  rapid  that  the  ventricle  is  unable  to  respond  to  each  im- 
pulse so  that  the  ventricular  rate  is  always  slower  than  the  auricular. 
The  abnormal  activity  may  occur  in  short  paroxysms  lasting  only  a 
few  minutes  or  may  be  continued  for  days  or  weeks.  It  seems  quite 
probable  that  this  peculiar  activity  differs  essentially  from  that  of 
auricular  paroxysmal  tachycardia  only  in  respect  to  the  rate  of  the 
auricular  contractions ;  in  paroxysmal  auricular  tachycardia  the 
auricular  rate  usually  does  not  exceed  250  per  minute  and  the  ven- 
tricles respond  to  each  auricular  stimulus ;  in  auricular  flutter  the 
auricular  rate  is  much  faster  and  the  ventricles  are  unable  to  re- 
spond to  each  auricular  stimulus. 

EXPERIMENTAL   PRODUCTION 

As  early  as  1887  MacWilliam*  described  the  phenomena  which 
result  from  the  application  of  a  weak  faradic  current  to  the  exposed 
auricular  wall  as  follows :  "It  sets  the  auricles  into  a  rapid  flutter 
.  .  .  the  movements  are  regular :  they  seem  to  consist  in  a  series 
of  contractions  originating  in  the  stimulated  area  and  thence  spread 
over  the  rest  of  the  tissue.  The  movement  does  not  show  any  dis- 
tinct sign  of  incoordination:  it  looks  like  a  rapid  series  of  contrac- 
tion waves  passing  over  the  auricular  wall."  Under  these  condi- 
tions the  ventricular  rate  is  accelerated  but  is  usually  one-half  or 
less  than  one-half  of  the  auricular  rate.     In  a  heart  beating  140  to 

*Jolly  and  Ritchie,  Heart,   1910-11,  ii,  77. 
♦Journ,  of  Physiology,  1887,  viii,  296. 

117 


i  [8  Auricular    Flutter 

iSo  per  minute  such  faradization  may  induce  an  auricular  rate  of 
500  to  600  per  minute  while  the  ventricular  rate  may  he  200  to  300 
per  minute,  [f  faradization  of  the  auricles  is  Stopped  the  "auricular 
flutter"  may  continue  fur  a  considerable  time  and  then  the  auricle 
may  resume  its  physiological  rate. 

in  the  frog's  heart  "auricular  flutter"  lasting  as  long  as  two  min- 
utes, starting  suddenly  and  terminating  abruptly,  may  he  induced 
by  a  single  induction  shock  applied  to  the  sinusf  or  some  portion  of 
the  auricle. $ 

While  the  auricles  are  in  "flutter"  vagus  stimulation  may  change 
the  flutter  into  a  condition  of  "fibrillation"  and  slow  the  ventricle; 
it  does  not.  however,  slow  the  coordinated  contractions  of  the  auricle. 
It  is  possible,  as  suggested  by  Ritchie,  that  excessive  stimulation 
of  the  accelerator  nerves  may  he  a  factor  in  producing  flutter  in 
an  otherwise  healthy  heart. 

MECHANISM 

Experimental  and  electrocardiographic  evidence  indicates  that 
auricular  flutter  is  characterized  by  a  rapid  rhythmic  series  of  auricu- 
lar contractions  having  their  origin  in  some  point  of  the  auricular 
musculature  other  than  the  sinus  node.  Nearly  all  paroxysms  of 
auricular  flutter  are  preceded  and  followed  by  extrasystoles  which 
interrupt  the  physiological  rhythm  more  or  less  frequently ;  the 
extrasystoles  are  auricular  in  origin  and  prohably  arise  in  the  wall 
of  the  upper  chamber  at  a  point  which  becomes  the  pacemaker  for 
the  paroxysm.  That  the  irritability  of  this  point  is  very  great  may 
be  concluded  from  the  great  rapidity  of  the  auricular  systoles.  The 
mechanism  is  the  same  as  that  of  auricular  paroxysmal  tachycardia 
but  in  flutter  the  auricular  rate  is  so  great  that  the  capacity  of  the 
bundle  of  His  to  convey  stimuli  is  exceeded  and  the  ventricle  re- 
sponds only  to  every  second  or  third  auricular  impulse.  In  most 
cases  the  ventricular  response  is  perfectly  rhythmic  and  there  is  one 
ventricular  contraction  to  two  or  three  auricular  contractions.  Less 
commonly  the  ventricular  contractions  are  arrhythmic  and  respond 
at  one  time  to  each  second  auricular  impulse,  at  another  time  to  each 
third  or  fourth  impulse  from  the  upper  chamber. 

fLoven  :  Mitteilungen  vom  physiol.  Laboratorium  in  Stockholm,  1886,  iv,  16. 
JEngelmann;  Arch.  f.  d.  gcs.  Physiol.,  1897,  lxv,  109. 


Auricular   Flutteb 


ng 


A. 


']/s 


1111 1  111, 11 1  iniimT 
ninumiiininii 


N     \ 


m 


Figure  8i 


Paroxysm    of   auricular    flutter.     During   the    attack   tlie    auricles    contract   rhythmically. 

The  ventricles  contract  rhythmically  at  a  slower  rate,  the  ventricle  responds  to  every  third 
auricular  impulse. 


iiuuiiumiuini 

mnrrrnrrnnrrrr 


Y, 


m 


ttl 


H 


s; 


Figure  82 


Paroxysm  of  auricular  flutter  with  irregular  ventricular  response.  Such  an  extreme 
grade  of  ventricular  irregularity  may  simulate  the  activity  of  auricular  fibrillation,  or  a 
lower  grade  of  irregularity  may  be  mistaken  for  extrasystoles.  The  ventricle  responds 
to   the   first,    second,   third   or   fourth   auricular   impulse. 

Diagrams  to  illustrate  the  mechanism  of  auricular  flutter  of  different  types.  The  arrows 
indicate  the  points  of  origin  and  direction  taken  by  the  stimuli.  Dotted  arrows  indicate 
the  time  at  which  the  normal  stimuli  at  the  sinus  node  should  reach  maturity  if  its  for- 
mation were  not  interrupted  by  the  abnormal  impulse  starting  from  a  lower  point  in  the 
auricle  and  traveling  upward.  The  thickness  of  the  lines  representing  ventricular  sys- 
tole indicate  the  relative  effect  of  the  several  contractions  in  maintaining  an  adequate 
circulation.  The  obliquity  of  the  A-V  line  indicates  the  varying  length  of  the  conduc- 
tion time.  As  =  auricular  systole.  A-V  =  conduction  from  the  auricle  to  the  ventricle. 
Vs  —  ventricular  systole. 


i-'o  Auricular   Flutter 

The  activity  may  be  regarded  as  an  auricular  tachycardia  with 
a  functional  depression  of  the  property  of  conduction  in  the  A-V 
bundle.  We  conclude  that  a  real  depression  of  conduction  exists 
because  we  know  that  in  "paroxysmal  tachycardia"  the  ventricle  mav- 
respond  to  the  auricular  impulses  at  a  rate  above  -'30  per  minute, 
yet  in  "auricular  flutter"  the  rate  of  the  lower  chamber  of  the  heart 
is  usually  not  above  120;  rarely  it  attains  a  rate  of  160  per  minute. 
Ritchie*  has  reported  a  patient  with  a  ventricular  rate  at  times  under 
40;  in  this  case  there  was  probablv  an  organic  lesion  of  the  bundle 
of  His. 

Figure  81  shows  in  diagrammatic  form  the  mechanism  of  a  par- 
oxysm in  which  the  ventricle  responds  rhythmically  to  every  third 
auricular  impulse;  during  the  attack  the  ventricular  rate  is  accele- 
rated but  is  only  one-third  the  rate  of  the  auricle.  Each  ventricular 
systole  of  the  paroxysm  is  less  forcible,  since  the  property  of  con- 
tractility has  not  had  the  same  time  to  recover  as  is  permitted  dur- 
ing the  physiological  rate.  The  exhaustion  of  the  capacity  of  con- 
duction in  the  A-V  bundle,  due  to  the  abnormal  shower  of  auricu- 
lar impulses,  is  indicated  by  the  obliquity  of  the  line  representing  the 
period  of  the  passage  of  the  stimulus  from  the  auricle  to  the  ven- 
tricle. 

In  Figure  82  are  plotted  the  auricular  and  ventricular  activities 
of  a  paroxysm  of  flutter  in  which  the  ventricular  response  is  very 
irregular;  the  lower  chamber  follows  the  first,  second,  third  or 
fourth  auricular  impulse  in  a  seemingly  haphazard  fashion.  The 
conduction  period  is  variable  and  prolonged.  The  ventricular  con- 
tractions have  a  force  proportional  to  the  preceding  diastolic  period. 
The  difficulty  of  differentiating  such  a  mechanism  from  that  of 
"auricular  fibrillation"  is  apparent.  If  the  ventricular  response  had 
been  rhythmic  up  to  the  time  of  the  final  beats  of  the  paroxysm, 
it  is  easy  to  see  how  the  pulse  and  heart  sounds  might  suggest  the 
occurrence  of  an  extrasystole  only. 

ETIOLOGY  AND   PATHOLOGY 

The  reported  cases  of  auricular  flutter  indicate  that  it  occurs  con- 
siderably more  often  among  men  than  women.  It  may  occur  at 
any  age;  the  earliest  subject  which  has  been  put  on  record  was  5 

^"Auricular  Flutter,"  London,  1914,  36. 


Auricular   Flutter 


121 


Jugular 


Carotid 


Brachial 


Figure  83 

Auricular   flutter  with   regular  ventricular   response.      Auricular   rate   276.      Ventricular 
rate  92. 


Jugular 


Carotid 


Brachial 


Figure  84 

Auricular    flutter    with    irregular    ventricular    response.     Auricular    rate    2S0.     Ventricle 
usually  responds  to  fourth  auricular  impulse,  at  X  it  responds  to  second  auricular  impulse. 


[22  A.URICULAR     FLUTTER 

years  old.  All  the  eases  which  I  have  observed,  with  one  excep- 
tion (14  years),  have  been  over  50  years  of  age.  Ritchie  in  his 
analysis  of  49  cases  found  that  70  per  cent,  occurred  after  the  for- 
tieth year. 

Auricular  flutter  rarely  occurs  without  some  other  evidence  of 
damage  t<>  the  cardiac  tissues  ;  about  a  third  of  the  cases  show  a  de- 
fect of  the  mitral  valve.  Dilatation  of  the  auricles  is  a  common 
antecedent  condition.  Pericarditis  has  been  present  in  several  cases. 
General  arteriosclerosis  in  which  the  coronaries  have  participated 
has  been  found  in  a  number  of  instances. 

The  acute  infections,  such  as  diphtheria  and  rheumatic  fever,  have 
been  the  evident  causative  agent  in  about  20  per  cent,  of  the  cases 
thus  far  reported.  Evidence  of  a  syphilitic  infection  is  obtained  in 
at  least  10  per  cent. 

It  has  been  suggested  that  an  abnormal  balance  of  external  ner- 
vous control  may  be  an  element  in  the  production  of  auricular  flut- 
ter, but  no  anatomical  lesion  which  would  indicate  a  removal  of 
vagus  influence  or  a  hypertonic  activity  of  the  accelerators  has  thus 
far  been  demonstrated. 

Such  evidence  as  is  at  hand  leads  us  to  believe  that  this  abnormal 
activity  has  its  origin  in  a  lesion  in  the  auricular  wall  which  con- 
stitutes a  focus  of  increased  irritability. 

In  the  few  post-mortems  which  have  been  reported,  in  those  who 
have  been  the  subjects  of  auricular  flutter,  histological  examinations 
have  failed  to  demonstrate  a  particular  focus  in  the  auricular  wall 
to  which  one  could  ascribe  the  functional  change,  but  general  in- 
flammatory and  degenerative  changes  of  the  myocardium  are  not 
wanting.  Dilatation  of  the  auricles  with  fibrous,  fatty  or  lymphocy- 
tic infiltration  of  the  walls  is  the  most  common  finding.  Atheroma 
of  the  coronaries  and  calcareous  deposits  in  the  arterial  wall  sug- 
gesting an  interference  with  the  nutrition  of  the  heart  musculature 
have  been  found  in  several  instances.  These  lesions  frequently  in- 
volve a  large  part  of  the  heart  muscle  and  may  include  the  sinus 
node  and  A-V  bundle.  Ritchie  (Case  III)  found  changes  in  the 
sinus  node  consisting  of  lymphocytic  infiltration.  Hemorrhage  and 
granular  degeneration  of  the  nodes  are  reported  by  Hume.*  I  have 
obtained  autopsies  in  three  cases,  men  of  51,  54  and  55  years,  re- 

♦Hcart,  1913-14,  v,  25. 


Auricular   Flutteb 


■R 

H 

MM 

,JL. 

*********  ***■**. 


fatient  II.  S.     Lead  I. 


jflGURE  55 

Auricular  flutter.     Time  lines  =  1/ 


Figure  87 

Patient    H.    S.     Lead   III.      Auricular  nutter.      Time   lines  =  1/^5   second. 
Figures  85,  86,   and  87  taken  from  the  same  subject.     Auricular  rate   336  per  minute. 
Kegular  ventricular  response  to  every  fourth  auricular  impulse,  ventricular   rate  84. 


i_>4  Auricular   Flutter 

spectively.     Each  showed  sclerosis  of  the  coronaries  and  extensive 
fibrous  myocarditis;  in  each  very  little  normal  heart  muscle  could 

he  found.     Each  had  an  old  infarct  of  the  left  ventricular  wall. 

IDENTIFICATION 

A  careful  history  and  physical  examination  may  lead  us  to  sus- 
pect "auricular  flutter,"  but  one  can  only  be  sure  of  the  correctness 
of  the  diagnosis  when  fortified  by  the  evidence  of  graphic  records. 
The  pulsation  of  the  veins  of  the  neck  gives  us  certain  information 
in  regard  to  the  activity  of  the  right  auricle,  a  very  rapid  rhythmic 
pulsation  of  the  jugular  vein,  showing  a  continuous  series  of  waves 
at  absolutely  equal  time  intervals  and  two  or  three  times  as  rapid 
as  the  ventricular  rate,  as  determined  by  auscultation,  suggests  an 
auricular  flutter,  but  it  is  quite  evident  that  by  mere  inspection  it  is 
most  difficult  to  count  and  correctly  determine  the  spacing  of  the 
small  venous  waves.  In  cases  of  established  auricular  flutter  I  have 
repeatedly  tried  to  elicit  auscultatory  evidence  of  the  rapid  auricu- 
lar activity  with  complete  failure. 

The  ventricular  contractions  may  be  perfectly  rhythmic  and  so 
accelerated  that  one  may  suspect  a  true  "paroxysmal  tachycardia" 
(see  Chapter  IX).  As  a  rule,  in  "auricular  flutter"  the  ventricular 
activity  is  less  rhythmic  and  not  as  fast  as  is  the  case  in  "paroxysmal 
tachycardia."  The  irregular  ventricular  activity  of  "flutter"  is  most 
often  mistaken  for  the  far  more  common  disturbance  known  as 
"auricular  fibrillation"  (see  Chapter  XI).  In  most  cases  of  "auric- 
ular flutter"  the  arrhythmia  is  not  as  great  as  in  "auricular  fibrilla- 
tion" and  in  the  latter  the  ventricular  form  of  the  venous  pulse 
may  aid  in  distinguishing  the  two  conditions;  however,  without  the 
assistance  of  graphic  records  the  separation  of  these  groups  is  prac- 
tically impossible. 

When  the  ventricular  rate  is  only  40  or  less  and  perfectly  rhyth- 
mic, one  at  once  suspects  a  condition  of  heart  block.  If  in  such  a 
case  the  jugulars  are  pulsating  rhythmically  at  a  rate  of  200  or  more 
per  minute,  one  can  be  reasonably  sure  that  a  condition  of  "auricu- 
lar flutter"  coexists. 

There  are  certain  types  of  irregular  ventricular  response  when 
the  auricle  is  in  flutter  which  simulate  forms  of  extrasystolic  ac- 
tivity.   For  example,  if  for  considerable  periods  there  is  a  ventricu- 


Auricular    Flutj  i:i< 


[2< 


:      :      :      .            : 

1 

•R        -R.       *. 

s 

pj^i^ 

s 

iiii 

1 

Figure  88 

Auricular  flutter.     Lead   I.     Auricular  rate   332.     Ventricular   rate    166.     As:Vs::2:i. 
Time  =  1/25   second. 


, ■ — ■  j 

1  .  — 1 


££dt*2JLE 


****** 


Figure  89 

Auricular  flutter.     Lead  II.     As:Vs::4:i.     As  =  492.     Vs  =  123.     Time  =  0.2  second. 


Figure  90 

Auricular     flutter     with     irregular     ventricular     response.       Lead     III.       As  =  280. 
Time  =  0.2  second. 


[26  Auriculas   Flutter 

lar  response  to  every  third  auricular  impulse  and  this  established 

rhythm  is  broken  by  a  ventricular  response  to  the  second  auricular 
impulse,  which  is  in  turn  followed  by  a  ventricular  contraction  after 
four  auricular  systoles,  the  early  beat  and  the  succeeding  pause  may 
give  one  the  impression  of  an  extrasystole  with  a  compensatory 
pause   ( see  Figure  82  |. 

The  polygram  is  often  of  material  aid  in  making  a  diagnosis  of 
auricular  flutter  and  the  jugular  tracing  may  demonstrate  the  rapid 
rhythmic  activity  of  the  right  auricle.  The  analysis  of  the  jugular 
curve  is,  however,  often  obscure,  since  the  record  of  the  waves  of 
auricular  activity  is  distorted  by  the  c  and  v  waves  characteristic  of 
the  normal  venous  tracing.  We  should  bear  in  mind  that  the  a,  c, 
:•  and  //  waves  of  the  normal  jugular  pulse  do  not  follow  one  an- 
other at  exactly  equal  intervals  of  time,  and  when  we  can  detect 
in  the  jugular  record  such  a  rhythmic  series  of  waves  two,  three 
or  four  times  as  rapid  as  the  ventricular  rate,  we  have  strong 
grounds  for  suspecting  a  condition  of  auricular  tachycardia. 

Figure  83  was  secured  from  a  case  of  "auricular  flutter"  in  which 
there  were  regularly  three  auricular  contractions  to  one  ventricu- 
lar. The  ventricular  rate  was  92,  the  auricular  rate  276  per  minute. 
One  of  the  a  waves  of  each  cycle  is  simultaneous  with  the  c  wave. 
The  ventricle  contracts  in  perfect  rhythm. 

A  type  of  irregular  ventricular  response  is  shown  in  Figure  84. 
The  jugular  record  is  composed  of  a  rhythmic  series  of  a  waves  at 
a  rate  of  280  per  minute,  which  can  be  picked  out  by  careful  meas- 
urement ;  the  pure  auricular  record  is  distorted  by  c  and  v  waves  of 
each  cycle  and  the  whole  is  superimposed  on  the  respiratory  curve. 
The  ventricle  is  contracting  at  a  rate  of  102  per  minute  ;  the  ventricle 
usually  responds  to  the  fourth  auricular  impulse,  but  occasionally 
(at  X)  it  responds  to  the  second  auricular  impulse.  This  type  of 
irregular  ventricular  response  would  strongly  suggest  occasional 
auricular  extrasystoles  were  it  not  for  the  evidence  obtained  from 
the  jugular  tracing.  The  analysis  of  both  of  these  polygrams  was 
verified  by  electrocardiographic  records  taken  at  the  same  time. 

The  electrocardiogram  must  be  our  final  court  of  appeal  in  sub- 
stantiating a  diagnosis  of  "auricular  flutter."  Even  here  the  evi- 
dence is  sometimes  obscure,  and  it  is  wise  to  have  records  taken  by 
the  three  standard  leads  in  order  to  be  certain  of  our  interpretation. 


Auricular   Flutter 


'-7 


PHI 


^*^^^\^^NnW^aI 


Auricular  flutter.      Lead   III.      Irregular   ventricular   response.     One   ventricular  extra- 
systole.     Time  =  1/25   second. 


*  R 


7K        K 


!^iJ^^I^Jf^Jr^!^^^j 


Figure  92 

Auricular  flutter.     Patient  H.     Auricular  rate  388.      Regular  ventricular   response  rate 
194.    Time  =  0.2   second. 


mmJ'pwmmnmmt  m&mmm  I 


T* 


IK 


mmmm  **mmmmmmrm 


A 


'- 


Figure  93 
TimeA=rIi2IaSecond!lati0n'     ^^  *""*  ""*  PEtient  (H°  as  Figure  9"' but  I5  da>"s  Iaten 


128  Auriculae    Flutter 

Figures  85  (lead  I),  86  (lead  II)  and  87  (lead  III)  were  taken 
from  the  same  patient  at  intervals  of  about  one  minute  and  indicate 
the  differences  in  the  records  secured  by  different  derivations.  Us- 
nallv  the  analysis  is  most  easily  made  from  leads  Jl  and  111,  but 
this  is  not  always  the  ease.  In  these  records  the  ventricle  is  beat- 
ing rhythmically  at  a  rate  of  84  per  minute  ;  the  auricle  is  contracting 
at  a  rate  of  336  per  minute.  (  >ne  of  the  auricular  (P)  waves  of 
each  cycle  is  submerged  in  the  R  defection  of  the  ventricular  cycle. 
The  T  wave  of  the  ventricular  complex  is  evident  only  in  leads  I  and 
11  as  a  slight  distortion  of  the  rhythmically  recurring  P  waves. 

In  Figures  88,  89,  90  and  i)i  are  shown  four  records  from  four 
distinct  cases  of  auricular  flutter  indicating  the  variations  which 
such  a  group  of  cases  may  present. 

In  l;igure  88  is  reproduced  a  curve  taken  from  a  patient  by  lead  I. 
In  this  instance  the  ventricular  rate  is  166;  the  auricular  rate  is 
332  per  minute.  The  ventricular  and  auricular  complexes  are  in 
part  superimposed  so  that  the  analysis  at  first  glance  seems  obscure ; 
by  the  aid  of  records  taken  by  leads  II  and  III  (not  reproduced) 
we  could  clearly  establish  a  rhythmic  rapid  activity  of  the  auricle 
at  double  the  rate  of  the  ventricle.  The  question  arises  in  this  case 
as  to  which  of  the  auricular  stimuli  excites  the  activity  of  the  lower 
chamber.  We  cannot  answer  this  question  positively  but  we  have 
strong  evidence  for  presuming  that  the  earlier  of  the  auricular 
stimuli  (PJ  is  the  one  to  which  the  succeeding  ventricular  contrac- 
tion is  the  response.  If  the  response  was  to  the  stimulus  delivered 
at  P2  the  conduction  time  (P»-Q)  would  be  abnormally  short. 
While  it  is  not  inconceivable  that  in  certain  cases  the  property  of 
conduction  may  be  heightened,  all  our  experience  goes  to  show  that 
in  those  cases  of  auricular  flutter  in  which  we  have  positive  evidence, 
conduction  is  normal  or  depressed  (usually  the  latter).  It  is  never 
demonstrably  shortened,  hence  we  are  led  to  believe  that  in  every 
case  the  conduction  time  is  longer  than  the  normal  and  therefore 
in  the  instance  shown  in  Figure  88  it  is  probable  that  the  ventricle 
responds  to  Px  rather  than  to  P.. 

A  case  in  which  the  lower  chamber  response  follows  four  auricu- 
lar contractions  is  depicted  in  Figure  89.  The  ventricular  rate  is 
1 23  ;  the  auricular  rate  is  492.  Both  chambers  contract  rhythmically, 
but  the  auricle  four  times  as  often  as  the  ventricle. 


Auricular    Flutter 


129 


~~ ! 1 r*-u  f"r^:"^T" 

71         H  "R 


R  "R 


fiBl 


p    P   T>    I     p  pi  p    p 


Figure  94 

Patient  K.     Auricular  flutter  with  irregular  ventricular  response  and  ventricular  extra- 
systole.     Time   1/25   second. 


Figure  95 

Patient  K.     Sequential  rhythm  taken  from  same  subject  as  Figure  94.     Taken  11  days 
later.     Note  same  type  of  ventricular  extrasystole.     Time  1.  25  second.    , 


130  Auriculas   Flutter 

Irregular  ventricular  responses  arc  shown  in  Figures  90  and  or. 
In  Figure  90  the  auricle  is  beating  rhythmically  280  times  per 
minute:  the  ventricle  responds  to  every  second  or  third  auricular 
stimulus. 

In  Figure  91  the  response  is  to  the  second,  third  or  fourth  auricu- 
lar stimulus.  This  record  is  further  complicated  by  an  unusual  com- 
plex indicating  one  ventricular  heat  having  its  origin  in  a  point 
in  the  ventricular  wall  quite  different  from  the  other  ventricular 
contractions,  which  are  of  supraventricular  origin. 

A  record  from  a  case  of  "flutter"  with  a  very  rapid  rhythmic  re- 
sponse is  represented  in  Figure  <  >2.  The  auricular  rate  is  38S ;  every 
other  auricular  complex  is  submerged  in  a  ventricular  complex  which 
occurs  194  times  per  minute.  The  ratio  of  the  rate  of  the  upper  to 
the  lower  chambers  is  as  2  is  to  I.  A  record  from  the  same  case 
1  Figure  93)  taken  15  days  later,  after  the  patient  had  taken  digi- 
talis, shows  complete  irregularity  and  a  rate  of  46  per  minute.  There 
are  at  this  time  no  coordinated  contractions  of  the  auricle,  but  its 
activity  is  one  of  "fibrillation." 

CLINICAL  COURSE  AND  SIGNIFICANCE 

Auricular  flutter  is  occasionally  the  only  evidence  obtainable  of 
a  defective  myocardium,  though  quite  commonly  extrasystoles  pre- 
cede and  follow  the  paroxysms.  In  such  patients  careful  examina- 
tion fails  to  reveal  any  organic  change  in  the  valves,  endocardium  or 
pericardium,  and  the  only  evidences  of  functional  disturbance  are 
those  elicited  during  the  paroxysm.  During  the  attack,  which  comes 
on  abruptly  and  terminates  suddenly,  the  patient  may  be  very  un- 
comfortable. He  is  conscious  of  an  unusual  commotion  in  the  chest ; 
the  accelerated  and  irregular  activity  of  the  ventricle  may  be  the 
cause  of  considerable  apprehension  ;  this  may  be  accompanied  by 
some  dyspnoea,  precordial  distress  and  prostration  if  the  paroxysm 
is  prolonged.  Some  attacks  may  extend  over  days  or  even  weeks, 
the  earlier  alarm  and  dyspnoea  may  subside,  and  the  patient  may  re- 
sume his  usual  occupation  aware  only  of  the  continuing  "palpita- 
tion." 

In  most  cases  there  are  other  evidences  of  myocardial  damage 
and  the  "auricular  flutter"  throws  an  additional  load  on  a  heart 


A  [jriculab    Flutter 


131 


1  1 

T>      P     P      P     P       P     P       P    P      P    P 

.^/****»  y^****  fa/"**""* 


d       f....f.     ' ''       '       ■?.    .   tm      a,.    „y 


Figure  96 

Patient   M.   K.     March    11,    1912.     Auricular   flutter.      Time   0.2   second. 


Figure  97 

Patient  M.  K.     December   12,   1914.     Sequential  rhythm.     Time  0.2  second. 


Figure  98 

Patient  M.  K.  December  2S,  1914.  Auricular  fibrillation.  Figures  96.  97  and  9S  are 
taken  from  the  same  subject,  the  first  of  these  was  taken  during  an  attack  of  pneumonia 
2    1/2  years  before   the   subsequent   records. 


132  Auricular   Flutter 

already  overtaxed.  In  such  patients  the  general  signs  of  cardiac 
insufficiency  may  have  been  present  before  the  onset  of  the  auricu- 
lar acceleration,  or  the  unusual  stress  occasioned  by  the  new  rhythm 
may  be  too  much  for  a  heart  barely  able  to  preserve  an  adequate 
blood  stream:  its  narrow  margin  of  safety  is  quickly  exhausted,  and 
sigm  and  symptoms  of  cardiac  insufficiency  rapidly  appear.  The 
extent  and  severity  of  the  symptoms  depend  to  a  very  large  degree 
on  the  condition  of  the  heart  before  the  attack;  the  auricular  flutter 
may  last  for  days  or  weeks,  yet  ultimately  the  heart  may  recover  a 
normal  rhythm  and  perform  its  work  with  reasonable  efficiency;  or 
in  a  short  time  there  may  develop  dyspnoea,  congestion  of  the  liver 
and  lungs,  edema  of  the  extremities,  Cheyne-Stokes  respiration, 
giddiness,  unconsciousness  and  collapse. 

A  patient  may  have  many  attacks  of  auricular  flutter  or  it  may 
appear  only  as  a  terminal  event.  Once  established,  the  attacks  are 
prone  to  recur  and  each  one  is  apt  to  persist  for  a  longer  time.  Oc- 
casionally one  sees  attacks  of  flutter  alternating  with  periods  of  nor- 
mal rhythm;  more  often  "auricular  flutter"  passes  into  "auricular 
fibrillation,"  which  may  persist  indefinitely  or  may,  in  turn,  give 
way  to  a  physiological  rhythm.  With  a  return  to  a  normal  rhythm 
the  symptoms  usually  improve. 

The  tendency  to  resume  a  normal  rhythm  is  seen  in  Figures  94 
and  95,  taken  from  the  same  patient  at  intervals  of  eleven  days. 
Figure  94  shows  auricular  flutter  at  300  per  minute,  with  an  ir- 
regular ventricular  response  interrupted  at  X  by  a  ventricular  extra- 
systole.  In  Figure  95  is  seen  the  sequential  rhythm  of  eleven  days 
later  interrupted  by  an  extrasystole  of  the  same  type  as  that  which 
occurred  during  the  period  of  "flutter." 

Figure  96  was  taken  from  a  patient  during  her  first  paroxysm 
of  flutter,  which  had  its  onset  during  an  attack  of  lobar  pneumonia 
in  March,  1912.  In  December,  1914,  she  returned  to  the  hospital 
with  broken  cardiac  compensation.  Her  record  taken  at  that  time 
(Figure  97)  shows  a  sequential  rhythm.  A  few  days  later  she  be- 
gan to  fibrillatc  (Figure  98)  and  has  continued  this  condition  up  to 
the  present  time  (6  months  later). 

The  clinical  significance  of  auricular  flutter  lies  in  the  fact  that 
it  indicates  a  considerable  degree  of  damage  present  in  the  auricu- 
lar wall.    That  the  damage  may  be  temporarily  repaired  is  indicated 


Auricular   Flutter  [33 

by  the  recovery  of  normal  rhythm,  but  the  tendency  to  repeated  and 
more  severe  attacks  suggests  that  usually  the  repair  is  incomplete. 

The  welfare  of  the  patient  depends  to  a  large  degree  on  the 
dition  of  the  ventricle.  With  a  normal  ventricular  muscle  the  patient 
will  withstand  many  attacks  of  "auricular  tachycardia"  with  com- 
parative immunity.  With  a  damaged  ventricle  the  outlook  is  much 
less  propitious.  Unfortunately  the  myocardial  damage  is  rarely 
limited  to  the  auricle.  In  "auricular  flutter"  a  slow,  regular  re- 
sponse of  the  ventricle  is  favorable;  a  rapid,  irregular  ventricular 
response  makes  the  outlook  more  serious.  The  change  to  a  condi- 
tion of  auricular  fibrillation  and  a  slowing  of  the  ventricle  under 
digitalis  are  to  be  regarded  as  a  favorable  sequence  of  events.  The 
return  to  a  normal  rhythm  is  to  be  welcomed  but  by  no  means  as- 
sures complete  recovery. 


CHAPTER  XI 

Auricular  Fibrillation 

The  group  which  we  arc  now  to  consider  is  characterized  by  a 
"complete  irregularity"  of  the  pulse.  Waves  of  varying  sizes,  large 
and  small,  separated  by  intervals  long  or  short,  follow  each  other 
in  a  confused  succession.  The  pulse  is  absolutely  devoid  of  rhythm. 
The  closest  study  will  not  enable  us  to  predict  whether  the  next 
event  in  the  series  is  to  be  a  forcible,  or  a  weak  impulse,  a  pause 
short  or  long.  We  may  have  a  series  of  small  waves  separated  by 
unequal  intervals  occasionally  mingled  with  large  waves,  or  large 
and  small  waves  and  longer  or  shorter  pauses  may  be  jumbled  to- 
gether in  the  utmost  confusion. 

In  the  older  literature  this  pulse  has  been  described  and  labeled 
with  many  different  names,  "pulsus  arhytlunicus,"  "deficiens," 
"iuacqualis,"  "intermittens,"  "irregularis/'  it  has  been  called  the 
"mitral  pulse."  The  pulse  rate  may  be  fast  or  slow,  it  may  exceed 
200,  or  may  be  under  40. 

The  heart  shows  the  same  degree  of  irregularity,  indeed  by  aus- 
cultation the  absolute  irregularity  is  made  more  apparent  than  by 
palpating  the  radial.  The  heart  activity  is,  I  think,  best  described 
by  the  now  discarded  term  "delcrium  cordis."  The  apex  impulses 
are  unevenly  spaced,  and  forcible  and  weak  thrusts  are  mixed  in  an 
erratic  series. 

The  heart  sounds  show  the  same  absence  of  rhythm  both  in  time 
and  force.  They  vary  greatly  in  intensity.  Each  contraction  may 
be  represented  by  a  first  and  second  sound,  or  at  more  or  less  fre- 
quent intervals  the  first  sound  alone  is  audible  suggesting  that  the 
feeble  contraction  has  failed  to  open  the  aortic  valves. 

The  credit  of  separating  this  type  of  disordered  myocardial  func- 
tion from  others  belongs  in  a  very  large  degree  to  Mackenzie,*  who 
pointed  out  the  constant  association  of  the  "ventricular  form  of 
venous  pulse"  and  "complete  irregularity"  of  the  ventricle.  At  this 
time  he  ascribed  these  phenomena  to  a  paralysis  of  the  auricles. 
Later  he  amplified  his  views  in  a  paper  based  on  the  study  of  500 

♦Study  of  the  Pulse,  London,  1902. 

134 


Auriculas    Fibrillation  135 

cases. f  In  a  scries  of  subsequent:  papers  he  modified  liis  theory  of 
the  underlying  defective  mechanism,  and  since  he  was  led  to  bel 
that  the  auricle  and  ventricle  contracted  simultaneously,  he  assumed 
that  a  point  near  the  A-V  junction  was  the  source  of  the  impulse 
which  simultaneously  excited  both  the  upper  and  the  lower  cham- 
bers. He  further  assumed  that  this  abnormal  pacemaker  was  lo- 
cated in  the  node  of  TawaraJ  and  therefore  introduced  the  term 
"nodal  rhythm"§  to  designate  this  group. 

The  real  explanation  of  the  activity  of  the  completely  irregular 
heart  was  made  clear  by  the  electrocardiographic  studies  of  Roth- 
berger  and  Winterbergjj  and  of  Thomas  Lewis. ||  To  these  investi- 
gators, working  independently,  is  jointly  due  the  distinction  of  con- 
clusively demonstrating  that  in  these  cases  there  is  no  gross  auricu- 
lar contraction,  but  that  the  auricular  wall  is  in  a  continuous  state 
of  fibrillation.  To  those  who  are  interested  in  the  facts  upon  which 
their  conclusions  are  based  a  study  of  the  original  papers  is  com- 
mended. 

EXPERIMENTAL  PRODUCTION   AND   MECHANISM 

When  the  auricle  of  an  exposed  heart  is  faradized  the  coordi- 
nated contractions  of  the  chambers  as  a  whole  cease,  there  is  no 
auricular  systole,  and  the  muscle  wall  assumes  the  relaxed  condition 
of  diastole,  the  muscle  mass  is,  however,  not  at  rest,  it  manifests  a 
continuous  activity  which  consists  of  fine  irregular  waves  with  here 
and  there  a  sharper  twitching  movement.  The  movement  has  been 
likened  to  the  appearance  of  the  squirming  of  a  bunch  of  worms. 
This  is  what  is  known  as  fibrillation  of  the  auricle.  It  is  similar  in 
appearance  to  the  fine  fibrillary  movements  which  are  not  infre- 
quently seen  in  the  tongue.  When  such  a  condition  is  produced 
experimentally  it  is  accompanied  by  a  complete  irregularity  of  the 
ventricle,  a  venous  pulse  of  the  ventricular  form  and  an  electro- 

fAmer.  Jour.  Med.  Sci.,  1907,  exxxiv,  12. 

JQuart.  Jour,  of  Med.,   1907-8,   i,  39. 

§With  our  present  clearer  insight  into  the  mechanism  of  the  completely- 
irregular  pulse,  the  term  "nodal  rhythm"  should  not  be  used  in  this  con- 
nection. It  should  be  reserved  to  designate  a  rare  but  definite  cardiac  activ- 
ity in  which  the  pacemaker  is  located  in  the  A-V  junctional  tissues. 

flWien.  klin.  "Wochenschr.,  1909,  xxii,  839. 

IJHeart,  1909-10,  i,  306. 


1 36  Auriculas    Fibrillation 

cardiogram  which  shows  a  continuous  scries  of  small  irregular  de- 
flections, which  arc  met  with  in  no  other  condition,  and  arc  un- 
doubtedly due  to  the  abnormal  auricular  activity. 

Lewis  studied  3  horses,  each  having  complete  irregularity,  the 
electrocardiograms  were  similar  to  those  obtained  from  nun  with 
complete  irregularity.  On  quickly  opening  the  chest  the  auricles 
could  be  seen  in  a  condition  of  fibrillation,  and  the  ventricles  were 
contracting  in  the  characteristic  irregular  manner.  Cushney  and 
Edmunds,*  who  were  familiar  with  the  experimental  production  of 
auricular  fibrillation,  in  discussing  a  case  of  complete  ventricular 
irregularity  in  man  were  the  first  to  suggest  that  this  phenomenon 
might  be  associated  with  a  iibrillating  auricle. 

Auricular  fibrillation  has  been  produced  experimentally  by  in- 
creasing the  intra-auricular  pressure  (Lewis),  by  stimulating  the 
vagus  and  accelerator  nerves  (Morat  and  Petzetakis)  by  the  applica- 
tion of  heat  to  the  myocardium  (Lagendorff)  and  by  toxic  doses  of 
drugs,  digitalis  (Francois-Frank),  nicotine  (Pezzi  and  Clerc), 
pilocarpine  (Busquet). 

It  has  been  suggested  by  Lcwist  that  fibrillation  is  due  to  a  highly 
irritable  condition  of  many  points  in  the  auricular  musculature,  each 
of  which  "is  independently  and  spontaneously  elaborating  hetero- 
genetic  impulses,"  that  is  to  say  he  views  the  condition  as  closely 
allied  to  the  auricular  extrasystole,  but  instead  of  there  being  one 
irritable  point  there  are  many,  and  the  multiple  impulses  thus  set  free 
neutralize  or  reinforce  one  another  in  an  utterly  haphazard  fashion. 

Recently  GarreyJ  has  taken  exception  to  this  view,  and  substi- 
tutes the  theory  that  the  condition  is  due  to  many  small  blocks  be- 
tween the  fibers  of  the  auricular  musculature,  so  that  the  fibers  re- 
ceive their  stimuli  not  by  the  usual  paths,  but  in  such  a  manner  that 
the  stimuli  pass  slowly  from  cell  to  cell  by  a  circuitous  path,  thus 
causing  contraction  waves  in  a  shifting  series  of  ring-like  undula- 
tions. 

There  is  little  question  that  the  ventricular  contractions  are  the 
result  of  irregular  impulses  received  from  the  auricle  for  the  electro- 
cardiographic ventricular  complexes  are  usually  of  the  form  which 

*Amer.  Jour.  Med.  Sci.,  1907,  exxxiii,  67. 
^Mechanism  of  the  Heart  Beat,  London,  191 1,  p.  192. 
(Am.  Jour.  Physiol.,  1914,  xxxiii,  397. 


Auricular    Fibrillai  [on 


'37 


are  secured  from  stimuli  arising  in  a  point  above  the  level  of  the 

junctional  tissues.  There  arc  several  factors  which  may  have  an 
influence  in  determining  the  instant  at  which  the  ventricle  shall  re- 
spond: (a)  it  is  conceivable  that  a  stimulus  is  effective  only  when 
of  a  certain  magnitude,  and  that  such  a  size  is  only  attained  when  a 
considerable  number  of  minute  auricular  impulses  bombard  the 
junctional  tissues  at  the  same  instant,  (b)  this  constant  shower  of 
auricular  stimuli  may  have  a  modifying  effect  on  the  excitability  or 
the  conductivity  of  the  bundle,  (c)  the  underlying  disease  which  has 
caused  the  damage  to  the  auricular  musculature  may  not  have  left 
the  A-V  bundle  unscathed. 


h 
w 


* »   m    »   m  •    »    »    »»    »     ■    »    ;    »»»»*»»■ *    ********  *         *      *.*.*** 


BE 


S^S3S  WWW.  \\.  \ 


Figure  99 


Diagram  to  illustrate  our  conception  of  the  mechanism  of  auricular  fibrillation.  Aff 
dots  of  various  sizes  indicate  stimuli  of  various  magnitudes  arising  in  many  parts  of  the 
auricular  wall  neutralizing  or  reinforcing  or  blocking  one  another.  When  effective  the 
impulse  is  transmitted  through  the  junctional  tissues  (A-V)  and  the  ventricle  responds 
(Vs)  at  irregular  intervals  with  a  varying  degree  of  force,  roughly  proportional  to  the 
length  of  the  preceding  diastolic  period.  It  is  to  be  noted  that  the  auricle  is  in  a  state 
of  continuous  activity,  but  there  is  no  coordinated  contraction:  also  that  the  stimuli 
which  call  forth  a  ventricular  contraction  arises  in  a  point  above  the  ventricular  tissues. 


The  peculiar  susceptibility  of  cases  of  auricular  fibrillation  to 
stimulationf  of  the  left  vagus  and  the  drugs  of  the  digitalis  group 
suggests  a  distinct  change  in  the  functional  activity  of  the  junctional 
tissues. 

The  force  of  the  successive  ventricular  contractions  depend  mainly 
on  the  period  of  rest  which  precedes  any  particular  contraction,  thus 
permitting  a  more  complete  filling  of  the  ventricle  and  a  recovery 
of  its  contractile  power,  but  as  has  been  pointed  out  by  Einthoven 
and  Kortweg^  this  relationship  is  not  always  maintained,  hence 
other  factors  must  be  at  work  which  are  not  completely  understood. 

The  accompanying  diagram  (Figure  99)  portrays  in  a  graphic 
manner  the  conception  of  the  mechanism,  the  upper  reaches  of  the 
junctional  tissues  are  being  continuously  bombarded  by  a  shower  of 

fDraper  and  Robinson:  Jour.  Exp.  Medicine,  1911,  xiv,  217. 
JHeart,  1915,  vi,  107. 


1^8  Auricular    Fibrillation 

small  impulses  from  the  auricular  segments;  at  irregular  intervals 
these  stimuli  become  effective,  and  a  ventricular  activity,  irregular 

iu  time  ami   force,  is  the  result. 

PATHOLOGY 

Every  heart  showing  fibrillation  of  the  auricles  which  has  been 
exhaustively  examined  has  given  evidence  of  gross  or  histological 
damage  of  its  tissues,  but  as  yet  no  lesion  has  been  described  to 
which  we  may  definitely  attribute  the  abnormal  functional  activity. 
Grossly  one  finds  valvular  defects,  most  frequently  mitral  stenosis, 
hypertrophy  and  dilatation,  pericarditis  and  coronary  sclerosis. 
Mackenzie  early  in  his  studies  pointed  out  the  frequency  with  which 
dilatation  and  hypertrophy  of  the  auricles  is  met  with  in  these  cases. 
Histological  examination  almost  invariably  reveals  evidence  of  acute 
or  chronic  inflammatory  changes  of  the  myocardium,  leucocytic  in- 
filtration, or  fibrosis  and  atrophy  of  the  muscle  cells.  In  several 
instances  the  blood  supply  of  parts  of  the  auricular  wall  has  been 
found  deficient.  In  some  cases  structural  changes  have  been  de- 
scribed in  the  sinus  node  or  in  the  A-V  node,  in  others  these  tissues 
have  revealed  nothing  abnormal  to  the  most  thorough  search.* 

The  recognized  fact  that  fibrillation  of  the  auricles  may  be  only 
temporary  suggest  that  in  a  certain  number  of  cases,  the  cause  may 
be  a  toxin,  or  a  temporary  nutritional  disturbance. 

Since  it  has  been  shown  experimentally  that  over  distension  of  the 
auricle  may  lead  to  fibrillation,  it  seems  reasonable  to  suppose  that 
an  auricular  wall  damaged  by  disease,  under  the  stress  of  a  defective 
valve,  or  the  demands  of  a  general  arteriosclerosis,  may  readily  fall 
into  fibrillation.  This  would  explain  the  onset  in  a  large  number 
of  the  cases  that  are  seen  in  the  clinic. 

ETIOLOGY 

Auricular  fibrillation  is  met  with  in  all  decades  of  life,  but  is  ex- 
tremely rare  in  those  under  ten  years  of  age.  In  a  personal  experi- 
ence with  over  300  cases  I  have  seen  only  one  case  under  the  age  of 
ten.  A  curve  of  the  age  incidence  (Figure  100)  indicates  that  89  per 
cent,  of  the  cases  occur  between  the  ages  of  21  and  60.     The  first 

*Colin :    Heart,    1912-13,   iv,   221. 


AUKICULAK     FIBRILLATION 


'39 


sharp  elevation  occurs  during  the  years  when  rheumatism  is  preva- 
lent, the  second  elevation  occurs  in  the  decade  when  the  rheumatic 
period  overlaps  the  time  at  which  arterio  i<  lerotic  change  bei  ome  a 
prominent  feature. 

It  is  seen  more  frequently  in  men  than  in  women,  the  proportion 
being  about  2  to  1. 

The  association  with  mitral  disease  is  very  noticeable,  60  per  <  ent. 
of  the  cases  showed  a  mitral  stenosis,  with  or  without  mitral  incom- 
petence, in  5  per  cent,  there  was  evidence  of   mitral   insufficiency 


Dfteth. 

I  -10  11-r.O        1.1  -  so  ai-uo  VI  -  So  J~l  -  Imt  (,1  -  TO  71  -fo 


b» 


1  /  ^^   S  i\  1  > 

; —  J , r"  Nr J  ". 

'  \    I  1  I       \       1  I 

!/         ;                     I       \  I 
-: 1- 1 J- i V -; ■ 

I  /'  J  :  \  I 

'  /    '  '  I  \  ' 

i       /  !  i  1  •  \ 

_i / • «»_«._«_  -._> - - ■ —  \ — — 

1  J  1  1  1  1  !         \  i 

1       S  1  '  V.        ' 

1  I  !  J  :  !  |\ 

J ! ! 1 1 ! J — J 


Rheumatism 


Degenerative  changes 

Figure  100 

Age  incidence  of  300   cases  of  auricular  fibrillation   arranged  by  decades. 


without  stenosis.  In  a  few  eases  there  was  an  aortic  lesion  as  well 
as  a  mitral  defect.  In  only  7  instances  have  we  seen  fibrillation  in 
hearts  with  defects  of  the  aortic  valves  only. 

Distinct  evidence  of  one  or  more  attacks  of  acute  rheumatic  fever 
was  obtained  in  over  one-half  of  the  cases  studied.  The  well-known 
frequency  with  which  rheumatism  affects  the  mitral  valve  is  further 
evidence  that  this  disease  is  the  underlying  cause  of  the  myocardial 
defect.  It  is  not,  however,  common  to  see  auricular  fibrillation  dur- 
ing the  first  attack  of  rheumatic  fever,  the  damaged  heart  does  not 
usually  go  into  fibrillation  until  some  years  after  the  evidence  of  a 
valvular  defect  has  been  established.     This  phase  is  further  empha- 


140  Auricular    Fibrillation 

sized  when  we  compare  the  age  incidence  of  rheumatism  and  of 
fibrillation:  according  to  Church*  57  per  cent,  of  the  mitral  attacks 

of  acute  rheumatism  occur  under  the  age  of  20.  Our  chart  of  the 
age  incidence  of  fibrillation  shows  that  in  only  16  casest  did  the 
onset  occur  before  the  twentieth  year,  and  only  149  casesj  showed 
fibrillation  during  the  first  four  decades.  This  suggests  that  fibril- 
lation points  to  a  rather  advanced  degree  of  tissue  damage.  The 
stretching  of  the  injured  auricular  muscle  under  the  stress  caused  by 
a  defective  valve  may  well  be  an  important  factor  in  producing  this 
type  of  abnormal  function. 

We  have  seen  fibrillation  develop  during  the  course  of  a  lobar 
pneumonia  on  six  occasion>.^ 

In  several  casts  with  mitral  disease  the  original  lesion  could  be 
attributed  to  an  attack  of  scarlet  fever. 

Attacks  of  influenza  seem  to  be  the  only  etiological  factor  that 
could  be  obtained  in  some  of  the  patients.  The  most  careful  scrutiny 
of  a  case  now  under  observation  has  given  no  explanation  of  a  well- 
marked  mitral  stenosis  and  auricular  fibrillation  other  than  repeated 
attacks  of  grippe. 

We  have  seen  fibrillation  of  the  auricles  in  four  cases  of  Graves' 
disease,  two  of  these  gave  an  old  history  of  attacks  of  acute  rheu- 
matic fever  and  each  presented  evidence  of  a  mitral  stenosis. 

Aside  from  the  rheumatic  cases,  and  those  in  which  the  myocar- 
dial damage  may  be  attributed  to  one  of  the  acute  infections,  there 
is  a  considerable  group  which  includes  those  suffering  from  de- 
generative changes,  such  as  general  arteriosclerosis,  chronic  nephri- 
tis, emphysema,  etc.  This  group  is  composed  of  patients  who,  for 
the  most  part,  have  passed  their  fortieth  year,  and  in  it  males  largely 
predominate. 

Syphilis  and  alcohol  appear  to  be  prominent  etiological  factors  in 
this  group.  Many  of  these  have  no  discoverable  evidence  of  valvu- 
lar disease,  a  soft  blowing  systolic  murmur  in  the  mitral  area  is, 

♦System  of  Medicine:  Allbutt  and  Rolleston ;  Vol.  ii,  Pt.  1,  603. 
|8  per  cent,  of  those  having  a  rheumatic  etiology. 
X"  per  cent,  of  those  of  rheumatic  origin. 

§In  126  cases  of  pneumonia  carefully  studied  by  Dr.  A.  E.  Colin,  fibril- 
lation occurred   in   12  cases    (personal   communication). 


Auricular    Fibrillation  141 

however,  not  an  uncommon  feature.     Several  had  dilatation  of  the 

arch  of  the  aorta,  and  insufficiency  of  the  aortic  valves. 

IDENTIFICATION 

Clinical.  Palpation  of  the  radial  pulse  in  most  instances  is  suffi- 
cient to  permit  us  to  assign  this  group  of  cases  to  their  correct  cate- 
gory. The  complete  irregularity  is  at  once  evident,  the  pulse  beats 
are  irregular  both  in  time  and  force.  As  a  rule  the  stronger  beats 
follow  the  longer  pauses,  but  the  disorderly  sequence  of  large  and 
small  waves  separated  by  intervals  long  or  short,  allows  us  to  make 
a  very  strong  conjecture  as  to  the  kind  of  abnormal  cardiac  activity 
with  which  we  have  to  deal.  There  are  other  cases  in  which  the 
complete  irregularity  is  not  so  easily  detected  by  palpation.  When 
the  pulse  volume  is  diminutive,  when  the  pulse  pressure  is  relatively 
small,  the  recognition  of  the  unequal  size  of  the  successive  waves 
may  be  quite  difficult.  In  cases  with  a  rate  of  over  160  the  pulse 
waves  may  show  very  insignificant  differences  in  size,  and  the  time 
intervals  may  show  variations  only  to  be  detected  by  the  most  care- 
ful measurements  secured  by  instrumental  means.  There  are  cer- 
tain patients  with  pulse  rates  between  70  and  80,  and  with  the  waves 
placed  at  such  even  intervals  that  an  uncorroborated  examination  of 
the  radial  pulse  is  quite  insufficient  to  classify  it  as  one  of  complete 
irregularity. 

Before  going  farther  we  should  emphasize  the  point  that  while 
practically  every  case  of  "auricular  fibrillation"  is  characterized  by 
a  pulse  of  "complete  irregularity,"  there  are  other  conditions  which 
may  also  afford  a  "completely  irregular"  pulse  which  can  only  be 
differentiated  by  exact  instrumental  methods,  while  in  nineteen  out 
of  twenty  instances  a  "complete  irregularity"  of  the  pulse  correctly 
indicates  a  condition  of  "auricular  fibrillation,"  the  twentieth  may 
be  the  result  of  an  entirely  different  heart  activity.  The  types 
which  may  notably  give  rise  to  this  confusion  are  certain  "sinus 
arrhythmias,"  and  cases  with  very  frequent  extrasystoles,  particu- 
larly when  they  arise  from  several  points  in  the  heart  wall  (Figure 
120),  or  are  interpersed  with  short  runs  of  paroxysmal  tachycardia 
(Figures  79  and  80). 

If  the  veins  of  the  neck  are  prominent  inspection  will  show  that 
the  jugular  pulsations  are  synchronous  with  the  apex  beat,  no  pre- 


i4-'  Auricular   Fibrillation 

systolic  wave  can  be  seen,  the  venous  pulse  is  of  the  ventricular 
form. 

Auscultation  of  the  apex  will  corroborate  the  complete  irregu- 
larity discovered  in  the  pulse,  and  at  times  will  make  clear  an  irreg- 
ularity which  was  not  discovered  when  palpating  the  wrist.  The 
sounds  vary  greatly  in  intensity  and  follow  one  another  at  unequal 
intervals.  (  U'ten  the  heart  beats  are  far  more  numerous  than  the 
arterial  pulsations,  some  contractions  are  too  feeble  to  perceptibly 
increase  the  lumen  of  the  radial  artery,  and  others  fail  even  to  open 
the  aortic  valve.  These  latter  are  represented  by  a  first  heart  sound 
only,  the  second  sound  is  wanting. 

The  question  as  to  whether  the  aortic  valves  are  or  are  not  opened 
by  any  particular  ventricular  contraction  depends  on  the  rela- 
tive pressures  in  the  aorta  and  the  left  ventricle.  If  the  diastolic 
period  is  very  short,  the  contractile  power  of  the  ventricle  will 
have  had  little  time  in  which  to  accumulate,  at  the  same  time 
the  pressure  in  the  aorta  will  be  relatively  high.  Under  such 
conditions  the  valves  will  not  be  opened.  On  the  other  hand 
given  a  longer  pause  the  next  succeeding  ventricular  contraction 
will  have  recovered  its  contractility  to  a  greater  degree,  the  aortic 
pressure  will  be  relatively  low,  and  the  aortic  valves  will  be 
opened. 

In  some  cases  where  the  degree  of  irregularity  is  moderate,  it 
may  be  difficult  to  distinguish  this  from  a  condition  of  extra- 
systole.  It  is  helpful  in  such  cases  while  listening  to  the  heart 
beats  to  concentrate  the  attention  on  the  beats  which  occasion- 
ally occur  too  early,  and  which  simulate  the  premature  beat  of 
the  extrasystole,  the  diastolic  period  following  these  early  con- 
tractions of  complete  irregularity  usually  do  not  have  the  same 
length,  nor  as  a  rule  do  they  have  as  long  a  duration  as  that 
which  would  constitute  the  "compensatory  pause"  of  an  extra- 
systole,  and  thus  may  be  differentiated. 

If  valvular  defects  are  present  murmurs  are  usually  detected, 
but  at  times  their  character  is  cptite  different  from  those  heard 
before  the  inception  of  the  complete  irregularity.  If  the  heart 
is  beating  very  rapidly  the  murmurs  are  less  intense,  and  the 
sharp  snap  of  the  first  sound,  so  characteristic  of  mitral  steno- 
sis, may  become  muffled.     The  intensity  of  the  murmurs  vary 


Figure  102 


AJUUIJJUiJLLUJLLLUJLLUiJ-UJUJLLJUAJJJ^ 


Figure  103 


JJuUUUlUlLLLULLLJULLUJJJJUL^ 


Figure  104 


yLijcJn  i  |i  11  j  I  iiil  AAA  k  Lilt  I  LLLkJJJJLLLLIJ  I  k  M  kLk  I  kl  H  H  tt 


Figure  105 

Arttrial  tracings  from  cases  of  auricular  fibrillation  showing  the  great  variety  of  pulses 
which  are  seen.     All  of  these  records  show  complete  irregularity. 


144  Auricular   Fibrillation 

from  cycle  to  cycle.  The  more  forcible  beats  arc  accompanied 
by  relatively  loud  and  harsh  murmurs,  the  more  frequent  feeble 
contractions  by  murmur-  of  less  conspicuous  intensity. 

There  is  frequently  an  increase  in  the  intensity  and  duration 
of  the  mitral  diastolic  murmur.  It  may  also  assume  a  rougher 
quality.  This  may  be  explained  on  the  basis  of  the  increased 
volume  of  blood  under  considerable  pressure  in  the  right  auricle, 
which  is  possibly  distended  and  is  never  emptied  by  an  effective 
contraction. 

For  the  most  part,  the  time  relations  of  the  murmurs  remain 
as  before  the  change  to  complete  irregularity,  systolic  and  dias- 
tolic murmurs  continue  to  occupy  their  established  position  in 
cardiac  cycle.  Mackenzie  long  ago  pointed  out  one  exception 
to  this  general  rule,  namely,  the  disappearance  of  an  established 
presystolic  murmur  in  cases  of  mitral  stenosis  which  changed 
from  a  physiological  rhythm  to  one  of  complete  irregularity. 
11  is  explanation  of  this  phenomenon  assumed  that  the  presys- 
tolic murmur  of  mitral  stenosis  was  due  to  auricular  systole, 
and  that  the  failure  of  the  auricular  contraction  accounted  for 
the  disappearance  of  this  murmur.  While  this  phenomenon  is 
frequently  seen  it  is  not  invariable  as  has  been  evidenced  both 
by  the  ordinary  methods  of  eliciting  physical  signs*  and  by 
occasional  graphic  records  of  the  heart  sounds  which  may  be 
found  in  the  literature.  Authorities  are  not  at  all  agreed  that 
this  presystolic  murmur  is  due  to  auricular  systole,  and  the  per- 
sistence of  the  murmur  in  certain  cases  of  undoubted  auricular 
fibrillation  lends  support  to  the  view  that  other  explanations  of 
the  mechanism  of  the  production  of  this  murmur  may  not  be 
disregarded. 

The  character  of  the  complete  irregularity  of  the  arterial 
waves  are  clearly  brought  out  by  taking  a  tracing  of  one  of  the 
peripheral  arteries  (radial,  brachial  or  carotid),  and  by  means 
of  a  simple  graphic  record  of  this  kind  (see  Figures  101,  102,  103, 
104  and  105)  one  can  hardly  miss  a  correct  diagnosis. 

The  great  variation  in  the  size  and  time  intervals  of  the  ar- 
terial pulse  waves  is  shown  in  Figures  101,  I02  and  103.  In  Fig- 
ures 101  and  102  the  waves  are  for  the  most  part  of  large  volume, 

♦Hart,   Med.  Rec,   New   York,   191 1,  lxxx,  2. 


Auricular    Fibrillation 


i45 


Jugular 


Brachial 


/J_AJUUUULAJlJUbULJUU^^ 


[0.2  second 


Figure  106 

Auricular  fibrillation.  Great  variation  in  the  size  of  the  arterial  waves  and  the  inter- 
vals between  them.  Jugular  completely  irregular,  a  absent,  c  and  v  waves  fused.  Depres- 
sion x  absent. 


J^Cfu/ar 


'ThhAV-* 


£™clufcl 


0>\  MLt 


Figure  107 

Auricular  fibrillation.  At  certain  places  the  form  of  the  arterial  record  might  suggest 
an  extrasystole.  In  the  jugular  record  note  the  "ventricular  form"  of  the  venous  pulse,  the 
a  wave   is  absent. 


i^6  Auriculae   Fibrillation 

but  show  considerable  differences  in  force  and  time  intervals.  Fig- 
ure 103  shows  a  brachial  pulse  rate  of  138.     Many  of  the  smaller 

waves  could  not  bo  detected  by  palpation  of  the  radial  artery,  hence 
it  is  easilv  seen  how  a  count  of  the  radial  alone  would  have  been 
very  misleading  in  determining  the  rate  of  the  heart  heat.     Figures 

104  and  105  are  both  taken  from  cases  of  auricular  fibrillation.  They 
indicate  an  unusual  degree  of  rhythmicity,  but  careful  measure- 
ments will  slmw  that  the  uniformity  is  apparent  rather  than 
real.  In  both  of  these  records  there  are  waxes  which  a  casual 
observer  might  mistake  for  extrasystoles,  but  close  attention  re- 
veals not  only  a  lack  of  uniformity  in  what  one  might  take  to 
be  wa\  es  of  the  physiological  rhythm,  but  further  a  period  of 
very  inconstant  length  both  before  and  after  the  small  waves 
which  thus  differentiate  them  from  the  intervals  which  one  finds 
on  either  side  of  the  extrasystole  as  commonly  observed. 

Polygrams  make  the  diagnosis  still  more  clear  (see  Figures  106, 
107,  108,  109  and  no).  In  these  records  the  arterial  curves  show 
in  considerable  variety  the  features  that  have  already  been  dwelt 
upon.  In  addition  to  this,  the  jugular  reveals  features  which  are 
characteristic  of  this  form  of  irregularity.  It  is  itself  completely 
irregular.  The  time  intervals  between  the  waves  indicate  a  com- 
plete absence  of  rhythmicity.  The  size  of  the  waves  show  great 
variations,  which  are  quite  independent  of  the  phase  of  respiration  in 
which  they  occur.  Furthermore,  the  venous  pulse  is  of  the 
"ventricular  form,"  that  is  to  say  all  the  positive  waves  occur 
during  the  ventricular  systolic  period,  the  a  wave,  the  represen- 
tative in  the  normal  jugular  of  auricular  systole  is  absent,  c  and  v 
waves  may  be  made  out,  the  c  wave  usually  varying  in  size  pro- 
portional to  the  synchronous  ventricular  contraction.  The  v 
wave  is  usually  a  large  broad  elevation  which  frequently  begins 
earlier  than  the  v  wave  of  the  physiological  rhythm  and  may  be 
fused  with  the  preceding  c  wave  (Figures  106  and  109).  The 
explanation  of  this  phenomenon  is  found  in  the  distended  con- 
dition of  the  auricle  which  is  probably  never  effectually  emptied, 
hence  the  ventricular  pressure  is  more  readily  transmitted  by 
way  of  this  blood  column  to  the  large  veins.  This  feature  may 
be  further  emphasized  by  a  relatively  insufficient  tricuspid  valve. 
The  V  wave  is  promptly  terminated  by  the  opening  of  the  tri- 


Auricular    Fibrillation 


M7 


J':;:  ilat 


Brachial 


0.2  sei    1  d 


Figure  108 

Auricular  fibrillation   with   a  very  rapid  ventricular  response.     From  a  case  of  general 
arteriosclerosis   with   high   blood   pressure. 


Jugular 


Brachial 


0.2  second 


Figure  109 

Auricular  fibrillation  with  slow  ventricular  response.     Xote  absence  of  a  wave,  absence 
of   depression  x,  unusual   depth  of   v,   small   oscillations   during  diastole    iff). 


148  Auricular    Fibrillation 

cuspid  valve,  and  the  discharge  of  blood  under  abnormal  pres- 
sure in  the  auricle  into  the  ventricle.  An  examination  of  the 
several  polygraphic  records  indicates  the  variety  in  the  form  and 
time  of  the  beginning  of  the  v  waves.  As  a  general  rule  the  cases 
<>i'  auricular  fibrillation  of  long  standing  with  overdistended  auri- 
cles and  veins  show  a  tendency  for  the  r  wave  to  become  fused 
with  the  c  wave,  and  the  depression  x  may  entirely  disappear. 
The  unusually  deep  depression  y  seen  in  Figure  109  indicates  an 
unusual  fall  of  pressure  when  on  the  opening  of  the  tricuspid 
valves  the  contents  of  the  distended  auricle  are  poured  into  a  re- 
laxed and  dilated  ventricle. 

Figure  108  illustrates  the  kind  of  curves  often  secured  from 
the  cases  of  auricular  fibrillation  with  a  very  rapid  ventricular 
response  in  old  arteriosclerotic  cases,  the  pressure  changes  in 
the  brachial  and  radial  arc  often  quite  small,  and  it  is  difficult  to 
obtain  good  arterial  tracings. 

A  slow  ventricular  rate  is  recorded  in  Figure  109.  The  brachial 
waves  are  well  marked  and  extremely  irregular  at  a  rate  of  60 
per  minute.  In  the  jugular  tracing  there  are  seen  during  diastole 
some  very  small  waves  marked  ff.  These  minute  fluctuations  in 
venous  pressure  are  not  infrequently  obtained  in  auricular  fibril- 
lation when  the  ventricular  response  is  deliberate,  they  have 
been  ascribed  to  the  undulating  auricular  activity,  but  it  is  quite 
probable  that  they  are  due  to  vibrations  induced  in  the  vein  by 
the  pressure  of  the  cup  used  as  a  receiver. 

Synchronous  records  of  the  apex  beat  and  carotid  are  repro- 
duced in  Figure  110.  At  X  are  seen  weak  ventricular  contrac- 
tions, which  are  barely  forceful  enough  to  overcome  aortic  pres- 
sure, and  presumably  would  be  too  weak  to  be  detected  in  the 
radial. 

The  electrocardiogram  usually  merely  corroborates  the  evidence 
of  auricular  fibrillation  obtained  by  the  simpler  methods  of  exam- 
ination, but  in  certain  obscure  cases  the  electrical  records  are 
essential  to  a  correct  diagnosis.  We  have  seen  cases  that  have 
been  carefully  studied  by  skilful  clinicians  in  which  the  irregu- 
laris was  mistakenly  interpreted  as  due  to  auricular  fibrillation, 
and  under  vigorous  treatment  the  patients  grew  worse  rather 
than  better.     The  galvanometric  records  disclosed  the  fact  that 


Auriculas    Fibrillai  eon 


'49 


'VJVJVJvJSw^jH^JV-Jv. 

> '  * — — 1  \ 

K. 

Carotid 

'    X 

w^t 

E  ■     ■ ' 

MB  ■■' 

' 

H  1919 131!    IS 

h  f\  J\ 

! 

Apex 

X                       .x 

-J\JN — M 

\J 

LLUJjLL/UJJjULLLUJJ-AJjU^ 

0.2  second 

Figure  iio 

Auricular  fibrillation.     Apex  and  carotid  tracings.     At  x  the  weak  ventricular  contrac- 
tions are  barely  able  to  open  the   aortic  valves. 


150  Aubiculab   Fibrillation 

these  "complete  irregularities"  were  not  caused  by  "auricular 
fibrillation,"  and  a  proper  revision  of  the  treatment  resulted  in 
immediate  benefit  to  the  patient. 

The  distinctive  features  of  the  electrocardiagram  of  auricular 
fibrillation  are  : 

1.  Complete  irregularity  in  the  time  intervals  between  the 
ventricular  complexes. 

2.  An  absence  of  the  P  wave. 

3.  A  series  of  small  waves  which  are  continuous  throughout 
the  whole  cardiac  cycle. 

If  one  examines  a  number  of  electrocardiograms  from  cases 
of  auricular  fibrillation  such  as  are  shown  in  Figures  III,  112,  117, 
etc.,  the  first  thing  that  arrests  our  attention  is  the  unequal 
spacing  of  the  ventricular  complexes.  Some  show  this  in  a 
greater  degree  than  others,  but  an  absolute  rhythmieity  is  al- 
most* never  seen.  The  parallelism  between  the  irregularity  of 
tbe  ventricle  and  the  arterial  pulse  is  shown  in  Figure  in  in 
which  simultaneous  curves  of  the  galvanometer  and  the  pres- 
sures from  a  cuff  placed  on  the  brachial  are  recorded. 

If  we  study  the  ventricular  complexes  carefully  we  are  led  to 
the  conclusion  that  they  have  a  normal  form  save  for  some  dis- 
tortion produced  by  the  small  waves  of  auricular  activity  which 
are  present  during  the  whole  cardiac  cycle,  both  systole  and 
diastole.  The  ventricular  complex  may  or  may  not  be  introduced 
by  a  Q  deflection,  both  the  ascending  and  descending  limbs  of 
the  R  wave  are  sharp  and  abrupt,  5"  may  or  may  not  appear.  T 
is  usually  present,  the  curve  which  is  the  result  of  the  contrac- 
tion of  the  lower  chamber  has  the  same  characters  and  is  of  the 
same  duration  as  is  found  in  the  same  heart  when  the  rhythm  is 
of  the  physiological  type.  The  records  shown  in  Figures  121  and 
122  were  taken  from  the  same  patient,  Figure  121,  in  June,  1910, 
when  the  auricles  were  contracting  efficiently.  Figure  122  was 
taken  10  months  later,  when  the  auricles  were  in  fibrillation.  A 
comparison  of  the  ventricular  portions  of  the  two  records  show 
a  marked  similarity,  the  R  and  T  deflections  are  of  the  same 
order,  and  of  the  same  duration.     We  must  therefore  conclude 

*An  exception  to  this  general  statement  is  seen  in  cases  of  auricular  fibril- 
lation complicated  by  an  .1-1'  Mock.    See  Chapter  XV. 


Auricular   Fibrillation 


15* 


Brachial 


Figure  hi 

Auricular  fibrillation.  Note  the  complete  irregularity  in  both  time  and  force  of  the 
brachial  waves.  The  ventricular  complexes  of  the  electrocardiogram  show  the  same  irregu- 
larity, the  P  wave  is  absent,  the  small  oscillations  (ff)  vary  greatly  in  size  and  duration, 
but    are   present   throughout    the    whole   cardiac    cycle. 


*Uwm 


n    n   n 


****** 


Figure  112 

Auricular  fibrillation  with  rapid  ventricular  response.  R  varies  in  height  according  as 
it  coincides  with  the  summit  of  one  of  the  small  waves  or  a  depression  between  two  small 
waves. 


i;-  Auricular    FIBRILLATION 

that  even  when  the  auricles  are  in  a  state  of  fibrillation  the  ven- 
tricles receive  their  stimuli  from  a  point  above  the  bundle  of  His, 
and  that  the  stimulus  travels  over  the  ventricle  by  a  path  that  is 
normal  in  all  respects.  The  ventricle  responds  to  a  supraven- 
tricular impulse. 

The  second  feature  of  importance  in  establishing  the  nature  of 
the  cardiac  activity  from  a  study  of  these  records  is  the  absence 
of  the  P  wave,  the  normal  representative  of  gross  auricular  con- 
traction. In  certain  records  (  Figures  117,  [23  and  127)  one  might 
at  first  glance  question  whether  in  some  of  the  cycles  a  wave  pre- 
ceding the  R  deflections  was  not  in  reality  a  P,  but  an  examina- 
tion of  a  number  of  cycles  will  soon  convince  one  that  the  incon- 
stancy in  the  size,  contour  and  time  relation  to  the  beginning  of 
ventricular  activity,  make  it  necessary  to  find  another  interpre- 
tation. 

In  the  electrocardiogram  of  the  normal  heart  it  may  be  re- 
called that  in  the  period  from  T  to  P,  the  diastolic  interval,  there 
is  a  line  without  any  suggestion  of  deflection.  In  the  records 
now  under  discussion  (Figures  1  1  1,  112,  113,  etc.)  this  period  is  evi- 
dently occupied  by  a  continuous  series  of  uneven  oscillations. 
These  are  the  representatives  of  the  rapid,  irregular  fibrillary 
activity  of  the  auricles.  Further  examination  will  convince  one 
that  these  small  deflections  are  not  limited  to  the  diastolic  pe- 
riod, but  are  continued  during  systole  as  well,  so  that  the  whole 
curve  is  modified  by  an  unending  series  of  these  small  fluctua- 
tions. It  is  for  this  reason  that  in  many  of  the  records  the  ven- 
tricular complexes  seem  to  lie  of  abnormal  form.  They  are 
merely  distorted  by  the  superimposition  of  these  representatives 
of  unceasing  auricular  activity.  The  T  wave  being  relatively 
small  is  frequently  very  much  changed  in  appearance.  The  R 
deflection  when  large  is  only  slightly  modified,  but  will  fluctuate 
in  height  (  Figures  1 1 1  and  112)  according  as  it  is  coincident  with  a 
summit  of,  or  a  depression  between  the  small  waves.  The  oscil- 
lations are  usually  arrhythmic,  and  vary  in  frequency.  When 
the  rate  can  be  estimated  it  will  be  found  to  be  between  400  and 
600  per  minute :  they  are  usually  most  conspicuous  in  records 
taken  by  the  second  and  third  leads. 

The  great  variety  in  the  rate,  size  and  rhythm  of  the  waves 


Auricular    Fibrillai  eon 


i53 


0.2  second 


Figure  113 

Auricular    fibrillation    with     ventricular     response     which     is    almost     rhythmic.       The 
auricular  oscillations  are  small,  but  distinct,   constant  and  quite   uniform   in  size. 


I 


S5- 


TV  !§ 


•R 


4/ 


0.2  second 


Figure  114 

Very   large   waves   of   auricular  activity   which    distort   the   ventricular   complex   to   a 
marked  degree. 


154  Auricular    FIBRILLATION 

of  fibrillary  activity  a^  shown  in  the  electrocardiogram  indicates 
great  differences  in  the  algebraic  sum  of  the  electrical  poten- 
tials developed  from  moment  to  moment  in  the  same  auricle, 
and  in  different  auricles.  The  oscillations  may  be  small  and  fairly 
rhythmic  throughout  the  whole  record,  as  seen  in  Figure  113,  or 
large  and  very  arrhythmic  (Figure  114).  Some  curves  show  a 
great  variation  from  cycle  to  cycle  (Figures  11  1  and  ii_>),  others 
small  fluctuations  which  are  inconspicuous  but  quite  constant 
(Figures  115  and  125).  One  may  at  times  be  confused  by  small 
rapid  oscillations  due  to  tremor  of  the  skeletal  muscles,  when 
during  the  recording  period  the  extremities  are  held  tense  and 
unrelated,  these  fluctuations  are  very  fine  and  much  more  rapid 
than  the  waves  of  auricular  fibrillation.  They  may  be  seen  in 
Figures  116,  117  and  118,  taken  from  the  same  patient  on  successive 
days  before,  during  and  after  a  paroxysm  of  auricular  fibrilla- 
tion. These  muscular  tremors  are  met  with  in  patients  under 
excitement  who  make  a  voluntary  effort  to  hold  themselves 
quiet.  If  the  rapidity  of  the  oscillations  are  noted  they  should 
not  be  confounded  with  the  waves  of  auricular  fibrillation  which 
have  a  much  slower  period  of  vibration. 

In  cases  such  as  are  shown  in  Figures  113,  114  and  115,  the  ar- 
rythmia  of  the  ventricles  is  only  moderate,  and  it  is  plain  that 
palpation  of  the  radial  or  auscultation  of  the  heart  might  fail  to 
reveal  the  "complete  irregularity."  The  graphic  records,  how- 
ever, make  clear  the  nature  of  the  abnormal  activity.  The  ven- 
tricle is  seen  to  be  definitely  arrhythmic,  P  waves  are  absent, 
and  the  continuous  series  of  oscillations,  large  or  small,  are  seen 
during  the  whole  cycle.  In  Figure  115  a  simultaneous  jugular 
curve  has  been  recorded.  In  this  may  be  noted  the  absence  of  the 
a  waves,  the  c  and  v  waves  participating  in  the  ventricular 
arrhythmia,  and  an  absence  of  the  depression  x  due  to  the  early 
onset  of  the  v  wave,  the  fine  oscillations  ff  are  also  apparent,  but 
as  has  been  pointed  out  in  an  earlier  paragraph  these  are  prob- 
ably not  characteristic  of  the  fibrillating  auricle,  but  are  due  to 
a  venous  thrill  induced  by  the  pressure  of  the  cup  used  as  a 
receiver. 


Auricular    Fibrillation 


00 


i 

y  *i 

i 

4£ 

T                               T 

r 

*«w^i»i 

T*                      *T 

.                 ;              .                      ..-,..,                   ■ 

Jugular 


jfl    Electro- 
cardiogram 


0.2  second 


Figure  115 

From  a  case  of  auricular  fibrillation  with  a  slow  ventricular  response.  The  form  of 
the  ventricular  complex  indicates  that  the  stimulus  which  called  it  forth  originated  in  the 
supraventricular  tissues.  P  is  absent.  R  and  T  are  but  slightly  distorted  by  the  super- 
imposed oscillations  of  auricular  activity  (ff).  Upper  curve  obtained  from  the  right  jugular 
vein,  a  is  absent,  c  and  v  have  coalesced. 


156  Auriculas   Fibrillation 

CLINICAL   FEATURES 

Practically  all  patient?  with  auricular  fibrillation  suffer  from 
some  degree  of  cardiac  insufficiency.  The  functional  disability 
of  the  heart  may  show  a  very  wide  range  in  different  patients, 
and  in  the  same  patient  at  different  times  it  may  vary  from  a 
condition  of  almost  complete  heart  failure  to  one  in  which  there 
is  ordinarily  no  evidence  of  an  inability  on  the  part  of  the  heart 
to  maintain  an  adequate  circulation,  and  in  which  symptoms  of 
insufficiency  develop  only  under  unusual  stress.  The  degree 
of  circulatory  embarrassment  depends  in  a  very  large  measure 
on  the  integrity  of  the  ventricular  muscle.  The  valvular  defect 
which  so  often  has  preceded  the  development  of  fibrillation  has 
thrown  upon  the  ventricles  abnormal  work,  and  perhaps  injury 
which  may,  however,  have  been  completely  met  by  a  compensa- 
tory hypertrophy.  More  often  the  underlying  disease  which  has 
damaged  both  valves  and  auricular  walls  has  also  attacked  the 
ventricles,  leaving  them  an  easy  prey  to  the  stress  which  the 
inception  of  the  new  rhythm  imposes.  If  therefore  the  ventricu- 
lar myocardium  is  extensively  damaged  one  may  expect  the  rapid 
development  of  the  classical  symptoms  of  cardiac  insufficiency, 
lowered  arterial  pressure,  increased  venous  pressure,  slow  capil- 
lary flow,  cedema,  cyanosis,  dyspnoea,  congestion  of  the  lungs, 
liver,  kidneys,  etc.,  etc.  On  the  other  hand  with  a  reasonably 
healthy  ventricular  muscle  the  strain  occasioned  by  the  disorder 
in  the  upper  chambers  may  be  supported  with  comparatively  little 
evidence  of  abnormal  blood  distribution. 

Fibrillation  once  established  usually  persists  to  the  end  of  life, 
hence  the  term  pulsus  irregularis  perpetuus,  which  was  formerly 
used  to  describe  the  arterial  features.  However,  one  sees  cases 
from  time  to  time  in  which  the  normal  pacemaker  reasserts  its 
control,  and  a  physiological  rhythm  is  regained.  This  has  oc- 
curred in  6  per  cent,  of  the  cases  which  have  come  under  my 
observation.  Such  a  case  is  shown  in  Figures  116,  117  and  118, 
taken  on  successive  days,  April  19,  20  and  21,  191 1.  The  records 
of  the  19th  and  21st  show  a  sequential  rhythm,  on  the  20th  (Fig- 
ure 117)  the  auricles  were  in  fibrillation. 


Auriculas    Fibrillation 


'57 


p  "P    ^       T  P 


Figure  116 

The  two  following  figures  were  obtained  from  the  same  patient  on  successive  days. 
April  ii),  191 1.  The  rhythm  is  sequential.  The  heart  is  rhythmic,  the  auricle  has  its 
normal  activity,   as   indicated  by   the   regular   appearance   of  the   P  deflection. 


Figure  117 

Same  patient  as  Figures  116  and  118.  Obtained  April  20,  191 1.  At  this  time  the 
auricle  was  temporarily  fibrillating.  Note  the  similarity  in  the  form  of  the  ventricular  com- 
pleves  in  these  three  records.  In  this  curve  P  is  absent,  there  is  complete  irregularity,  the 
small   deflections    (ff)    due   to  the   fibrillating  auricle   are   present. 


E=$3 

? 

m  *-* 

-  -i- 

i:  ■■:   : :. 

I  :Tl:~ 

Hi 

A 

\            J 

A    I 

T^JkJ  m 

-/*/ 

mS 

* 

L  . 

■ff* 

f*f| 

^^  ■■  1  J& 

*rV 

Y^r 

/ 

^^»    Tl 

Figure  118 

Obtained  from  the  same  patient  as  Figures  116  and  117,  on  April  21,  191 1.  The  auricle 
has  resumed  coordinated  contractions  and  the  rhythm  is  again  sequential.  In  all  three 
of  Khe  above  records  note  the  fine  rapid  oscillations  which  are  due  to  a  tremor  of  the 
skeletal  muscles. 


158  Auriculas   Fibrillation 

Under  ''paroxysmal  tachycardia"  reference  was  made  to  an  un- 
usual form  of  paroxysm  consisting  of  a  short  run  of  auricular 
fibrillation,  with  a  rapid  irregular  ventricular  response  interrupting 
an  ordinary  sequential  rhythm.  Such  a  paroxysm  is  shown  in  Fig- 
ure 119.  The  earlier  portion  of  the  record  shows  a  number  of 
cycles  during  which  the  sinus  node  is  evidently  the  pacemaker.  The 
rhythm  is  broken  at  A  by  an  auricular  extrasystole  ;  this  is  followed 
by  a  normal  cycle,  then  a  bizarre  curve  which  it  is  difficult  to 
classify,  but  which  may  possibly  represent  an  abnormal  ventricular 
contraction  and  two  ectopic  auricular  contractions;  these,  in  turn, 
are  succeeded  by  a  short  period  of  auricular  fibrillation  with  a 
rapid  irregular  ventricular  response.  The  paroxysm  of  fibrillation 
lasted  for  about  a  minute  and  the  sequential  rhythm,  broken  by 
occasional  auricular  extrasystoles,  reappeared.  Patients  showing 
this  condition  are  very  few  in  number,  and  in  my  experience  it 
is  very  unusual  to  secure  the  graphic  evidence  of  the  transition 
from  the  sequential  rhythm  to  the  paroxysm  of  auricular  fibrilla- 
tion. This  curve  was  obtained  from  a  patient  seen  in  consultation 
bv  Professor  Longcope  and  was  recorded  by  my  assistant,  Dr. 
Strong. 

These  paroxysms  may  appear  over  a  period  of  many  years.  A 
case  reported  by  Cushny  and  Edmunds  had  attacks  for  twenty 
wars.  Robinson*  has  reported  careful  studies  in  a  case  which  had 
probably   suffered    from   attacks    for   twelve  years. 

The  transitory  character  of  the  paroxysms  has  been  somewhat 
difficult  to  explain.  A  number  of  patients  in  whom  1  have  ob- 
served this  phenomenon  were  suffering  from  lobar  pneumonia ; 
here  it  is  quite  likely  that  the  toxins  of  the  disease  had  a  direct 
action  on  the  muscle  cell.  It  has  been  observed  in  hearts  which 
showed  no  other  clinical  evidence  of  a  pathological  lesion.  Macken- 
zie! nas  suggested  that  digitalis  may  be  a  possible  factor  in  caus- 
ing the  auricular  fibrillation.  Robinson  has  advanced  the  hypoth- 
esis that  in  certain  cases  the  paroxysm  may  be  due  to  an  altera- 
tion in  the  blood  supply  to  the  auricular  musculature.  He  also 
reports  a  casef  which  was  directly  attributed  to  poisoning  with 
hydrogen  sulphid. 

*Arch.   Int.   Med.,   1914,  xiii,  208. 
tHeart,   1910-1 1,  ii,  295. 


n* 


m 


H! 


ft 


to 


1 59 


U       2   - 


160  Auricular   Fibrillation 

The  patient  is  not  necessarily  conscious  of  the  irregular  heart 

action.  At  times  they  apply  for  examination  <>n  account  of  the 
sensation  vi  "fluttering"  or  "thumping"  in  the  precordial  region 
or  complain  of  "palpitation."    More  frequently  dyspnoea  or  oedema 

are  the  symptoms  which  bring  them  to  the  physician,  and  the 
erratic  and  tumultuous  heart  activity  has  passed  unnoticed.  Very 
few  of  them  complain  of  anginal  pains,  but  tenderness  in  the 
precordial  region  is  a  symptom  frequently  elicited  during  the  ex- 
amination with  the  ringer,  or  the  bell  of  the  stethoscope.  In  cases 
which  have  been  watched  over  a  long  period,  one  will  often  see  the 
following  series  of  events:  (i)  Several  attacks  of  rheumatic  fever 
with  arthritis  and  endocarditis,  most  frequently  involving  the  mitral 
valve.  (2)  Later  extrasystoles,  often  auricular  in  origin.  (3)  The 
heart  becomes  gradually  dilated  under  physical  stress,  and  the  auri- 
cles begin  to  fibrillate,  and  usually  continue  this  activity  up  to  the 
time  of  death,  which  may  be  postponed  for  many  years. 

Such  a  sequence  of  events  is  shown  in  Figures  121,  122  and  123. 
The  patient,  a  man  of  50,  had  a  sharp  attack  of  rheumatic  fever, 
followed  by  endocarditis,  when  he  was  20  years  of  age.  At  that 
time  he  was  seen  by  Dr.  E.  G.  Janeway,  who  told  him  he  had  a 
mitral  stenosis.  I  first  saw  him  in  1909,  when  he  became  conscious 
of  an  irregularity  of  the  heart.  At  that  time  the  rhythm  was  se- 
quential, but  he  had  occasional  extrasystoles,  which  were  verified 
by  polygraphic  tracings.  On  June  7,  1910,  the  curve  shown  in 
Figure  121  was  obtained.  It  shows  an  extrasystole  of  auricular 
origin,  and  a  split  P  wave.  During  an  attack  of  pneumonia,  in 
February,  191 1,  his  auricles  began  to  fibrillate.  Figure  122  was 
obtained  on  April  28,  191 1,  and  Figure  123  secured  April  9,  191 5. 
This  has  continued  up  to  the  present  time  (July,  1916).  He  is 
now  in  excellent  health,  and  is  able  to  conduct  a  business  involving 
large  responsibility,  but  slight  physical  exertion. 

The  rate  of  the  heart  beat  in  auricular  fibrillation  is  extremely 
variable.  One  sees  cases  in  which  the  rate  does  not  exceed  40  a 
minute,  and  others  which  exceed  200.  Under  appropriate  treatment 
it  is  not  unusual  to  see  a  rate  of  140  reduced  to  100  in  a  very  short 
time. 

tJour.  Amer.  Med.  Assn.,  1916,  lxvi,  161 1. 


Auriculae    Fibrillation 


JaJjI/  J&* — -J^^J^ 


c&ai 


FlGUKE    121 

Patient    B.   S.,  June   7,    [910.      The   auricle   is  contracting  as  a  whole.      P  is  broad  and 
split.      Kxtrasystule   of  auricular   origin   at   x.      Note   fine   tremor  of   skeletal    muscles. 


Figure  122 

Patient   B.   S.,  April  28,   191 1.     The  auricles  are   now  fibrillating,  the   rhythm  is   rapid 
and  very  irregular. 


Figure  123 

Patient  B.  S.,  April  9,  191 5.  Figures  ui,  122  and  123  are  all  from  the  same  subject. 
The  auricles  are  still  fibrillating,  but  "the  ventricular  response  is  much  less  rapid  and  more 
evenly  spaced. 


[62  Auriculas   Fibrillation 

The  palpation  of  the  radial  pulse  is  a  very  insufficient  criterion  of 
the  condition  of  the  circulation.  While  the  palpation  of  the  pulse 
alone  may  be  sufficient  to  establish  a  diagnosis,  and  while  by  this 
method  one  immediately  delects  the  complete  irregularity  in  force 
and  frequency  which  characterize  this  group,  the  count  of  the  radial 
pulse  may  be  misleading.  Frequently  the  number  of  the  impulses 
which  can  be  counted  at  the  wrist  is  far  below  the  actual  number  of 
cardiac  contractions.  Only  those  waves  which  are  of  considerable 
volume  and  force  can  be  felt  at  the  wrist  (see  Figure  125),  and  many 
small  ventricular  contractions  expend  their  force  before  reaching 
the  radial,  and  some  even  fail  to  open  the  aortic  valves.  These 
small  contractions  are  ineffectual  in  maintaining  an  adequate  circu- 
lation, yet  are  exhausting  to  the  heart  muscle,  for  we  know  that,  in 
accordance  with  the  law  discovered  by  Bowditch,  every  contraction 
of  heart  muscle  is  maximal,  that  is  to  say,  if  it  contracts  at  all,  it  ex- 
hausts all  of  the  energy  stored  as  contractile  material  in  its  muscle 
fibers  at  any  particular  moment ;  hence  it  is  evident  that  however 
small  a  contraction  may  be,  it  must  be  taken  into  consideration  in 
estimating  the  gravity  of  the  condition  of  any  particular  heart. 

The  inadequacy  of  the  observations  on  the  radial  pulse  alone  is 
well  illustrated  in  Figure  124.  Here  the  lower  margin  of  the  shaded 
area  indicates  the  radial  count.  If  one  were  guided  by  this  alone, 
one  would  have  said  that  on  admission  the  cardiac  rate  was  under  70 
and  never  above  100.  The  upper  boundary  of  the  shaded  area  is 
the  count  taken  by  auscultation  at  the  apex,  and  represents  much 
more  accurately  the  true  condition,  the  admission  rate  being  127; 
the  gradual  reduction  to  the  neighborhood  of  60  makes  the  real  im- 
provement apparent. 

The  term  "pulsus  deficiens"  has  for  a  long  time  been  used  in 
describing  pulse  phenomena  (Traube,  Hering,  Wenckebach,  etc.), 
but  each  author  has  used  it  with  a  different  meaning ;  some  have 
considered  it  synonymous  with  "pulsus  intermittens,"  others  have 
applied  it  to  an  absence  of  ventricular  contraction,  wdiich  breaks  the 
ordinary  rhythm ;  it  has  been  used  in  describing  extrasystoles  and 
pulse  alternans. 

By  "pulse  deficit"  we  mean  the  difference  between  the  number 
of  cardiac  contractions  and  the  number  of  impulses  which  can  be 
palpated  in  the  radial  artery.    The  best  way  of  determining  the  pulse 


Auricular    Fibrillation 


i63 


1 

01). 

130 
120 
110 
100 
00 
80 
70 
60 

104 

* 

103 
102. 
10f- 
100  i 

is     I     is          ii          it           in          u           ii 

A 

J      n.  :!::: 

I          ^MF^ft. 

■  1     ^^^> 

IP  ^     Vfe, 

98°  I 

Hr                  :"fff  thiJ«V— 

_oz! 

:::::::::::::::::::::::::::::::    :^ 

:__ 

oir.iT 

ALI9  INFUSION  4               6                        6                        C                        6                        0                        G 

Figure  124 

The  shaded  area  represents  the  pulse  deficit;  the  upper  edge  is  the  apex  rate;  the 
lower  edge  is  the  radial  rate.  Figures  in  digitalis  column  indicate  dosage  of  the  infusion 
in   drams  per  twenty-four   hours.     Patient  in  bed   during  period   represented    in   the   figure. 


Rrachial 


Figure  125 

Auricular  fibrillation.  Simultaneous  records  of  the  cardiogram  and  the  brachial  pulse. 
Showing  the  mechanism  of  the  "pulse  deficit."  Every  other  heart  beat  has  little  or  no 
effect  in  raising  the  pressure  i.i  the  brachial  artery. 


164  auricular    Fibrillation 

deficit  is  to  have  the  apex  counted  by  auscultation  by  one  observer, 
while  another  is  simultaneously  counting  the  radial  (these  observa- 
tions must  cover  a  period  of  not  less  than  a  full  minute,  on  account 
of  the  extreme  irregularity  of  the  pulse  in  many  of  these  cases  a 
count  of  one-quarter  or  one-half  minute  only  is  much  less  accurate). 
When  one  is  obliged  to  make  these  observations  unaided,  the  apex 
and  the  radial  counts  may  be  made  in  successive  minutes.  This  of 
course  does  not  give  an  absolutely  accurate  deficit,  but  it  is  extraor- 
dinary how  closely  the  counts  of  successive  minutes  will  coincide 
even  when  the  heart  and  radial  show  the  most  extreme  degrees  of 
irregularity.  After  a  little  practice  one  may  be  able  simultaneously 
to  auscultate  the  apex  and  palpate  the  radial,  thus  determining  the 
number  of  beats  which  fail  to  reach  the  wrist  in  the  period  of  a 
minute. 

In  Figures  124  and  126  the  upper  margin  of  the  shaded  area 
represents  the  apex  count,  the  lower  margin  the  radial  count,  and 
the  width  of  the  shaded  area  represents  the  deficit  at  any  particular 
point  in  the  curve. 

The  relative  deficit.  In  many  cases  of  auricular  fibrillation,  par- 
ticularly where  improvement  has  occurred  and  the  heart  has  become 
less  irregular,  slow,  and  fairly  compensated,  it  will  be  found  that 
the  count  at  the  apex  and  the  radial  are  identical.  Even  in  these 
c^-js  the  individual  waves  show  a  considerable  variation  in  force 
and  size.  This  is  brought  more  clearly  to  view  if  the  cuff  of  a  blood- 
pressure  apparatus  is  placed  on  the  arm  and  the  radial  is  counted 
while  varying  degrees  of  pressure  are  applied  through  the  cuff. 
This  difference  in  the  pressure  values  of  successive  waves  we  have 
termed  the  "relative  deficit,"  as  contrasted  with  the  absolute  deficit, 
when  without  brachial  pressure  some  waves  fail  to  reach  the 
radial. 

The  following  observation  will  serve  to  illustrate  this  point :  The 
patient  was  a  gentleman  who  had  fibrillating  auricles  for  something 
over  two  years,  with  at  times  an  apex  rate  of  160  and  an  absolute 
deficit  of  over  50.  Later  his  heart  was  fairly  compensated,  and  he 
was  able  to  supervise  large  business  interests  which  required  a  daily 
attendance  at  his  office  of  six  to  eight  hours.    When  we  last  saw  him 


Auriculae    Fibrillai  ion 


16s 


tta_ 


iihsaf     .d    .;!:::;::!!  ii:!::!;sii!;;ii....;;i..i 


.DIGITALIS'      0  S  3 


BL.  P.  SY3.1C0       ICO 


L^i 


:3 


ICO        102    j    ISO 


I 

:  ]  i/ii 


*  .*    I 


Figure  126 

The  shaded  area  represents  the  pulse  deficit:  the  upper  edge  is  the  apex  rate,  the  lower 
edge  the  radial  rate.  The  hroken  line  indicates  the  "average  systolic  blood-pressure" 
(compare  these  values  with  the  figures  at  the  bottom  of  the  chart,  which  show  the  systolic 
blood  pressure  determined  by  the  usual  method).  Figures  in  digitalis  column  indicate 
drams  of  the  infusion  per  twenty-four  hours. 


if/.  Auricular   Fibrillation 

his  apex  rate  was  64,  radial  rate  64,  deficit  o.     On  applying  the 
brachial  cut!  the  following  counts  were  obtained  : 


Brachial   pressure 

Radial 

count   per  minute 

140  nun.   Ilg. 

0 

130  nun. 

50 

120  mm. 

58 

no  nun. 

62 

IOO  nun. 

64 

While  he  had  no  absolute  deficit,  his  relative  deficit  was  quite  evi- 
dent when  the  pressure  values  of  the  waves  of  one  minute  were  thus 
studied.  This  relative  deficit  may  be  detected  in  all  cases  of  auricu- 
lar fibrillation  ;  it  is  rarely  seen  in  other  cardiac  arrhythmias.  We 
have  found  that  such  observations  on  the  relative  deficit  are  of  real 
diagnostic  value  in  corroborating  a  condition  of  auricular  fibrilla- 
tion which  palpation  and  auscultation  have  led  us  to  suspect. 

The  usual  way  of  estimating  blood  pressure  is  entirely  fallacious 
in  auricular  fibrillation.  The  accustomed  method  of  obliterating  the 
brachial  artery  by  cuff-pressure  and  then  by  gradually  lowering  the 
pressure  to  determine  the  systolic  blood-pressure  by  the  height  of 
the  mercury  column  at  which  the  pulse  wave  below  the  cuff  is  de- 
tected by  palpation  or  auscultation  is  obviously  of  little  value  when 
practically  each  pulse  wave  has  a  different  pressure  value. 

If  such  a  pulse  is  observed  for  a  period  of  a  minute  it  will  be 
found  that  only  a  small  fraction  of  the  total  number  of  cardiac  con- 
tractions have  a  pressure  value,  approximating  the  systolic  blood- 
pressure  as  determined  by  this  method.  Figure  126  illustrates  the 
inaccuracy  of  this  method  in  these  cases.  Systolic  blood-pressure 
taken  by  the  usual  method  would  signify  that  the  successive  blood- 
pressures  of  this  patient  were  165,  160,  160,  162,  156,  155,  148,  etc., 
and  that  as  her  condition  improved  the  blood-pressure  was  lowered. 
As  a  matter  of  fact,  only  a  few  beats  could  be  detected  below  the 
cuff  when  exerting  a  pressure  at  these  levels,  and  while  doubtless 
her  systolic  blood-pressure  was  momentarily  at  these  levels,  they  in 
no  way  indicate  the  efficient  pressure  of  the  blood  column.  As  we 
shall  show  later,  her  systolic  blood-pressure  really  increased  with  the 
improvement  in  her  condition. 

A  much  more  valuable  estimate  of  the  force  of  the  blood-slream 


Auricular   Fibrillation 


167 


can  be  obtained  by  estimating  the  blood-pressure  by  another  method  ; 
the  average  systolic  blood-pressure. 

To  obtain  what  for  convenience  we  have  termed  "the  average 
systolic  blood-pressure,"  the  apex  and  radial  are  counted  for  one 
minute,  then  a  blood-pressure  cuff  is  applied  to  the  arm,  and  the 
pressure  raised  until  the  radial  pulse  is  completely  obliterated;  the 
pressure  is  then  lowered  10  mm.,  and  held  at  this  point  for  one  min- 
ute, while  the  radial  pulse  is  counted;  the  pressure  is  again  lowered 
10  mm.,  and  a  second  radial  count  is  made ;  this  count  is  repeated  at 
intervals  of  10  mm.  lowered  pressure  until  the  cuff-pressure  is  in- 
sufficient to  cut  off  any  of  the  radial  waves  (between  each  estima- 
tion the  pressure  on  the  arm  should  be  lowered  to  zero).  From  the 
figures  thus  obtained  the  average  systolic  blood-pressure  is  calcu- 
lated by  multiplying  the  number  of  radial  beats  by  the  pressures 
under  which  they  came  through,  adding  together  these  products 
and  dividing  their  sum  by  the  number  of  apex-beats  per  minute, 
the  resulting  figure  is  what  we  have  called  the  "average  systolic 
blood-pressure."  The  following  two  observations  made  on  a  pa- 
tient will  indicate  the  method  of  computation : 

B.S.,  April  29,  1910.     Apex,  131 ;  radial,  101 ;  deficit,  30. 

Radial   count, 
o 
13  I3X90="70 

47—  13  =  34  X  80  =  2720 

75  —  47  =  28  X  70=1960 

82  —  75=    7X6o=    420 

101  —  82  =  19  x  50  =    950 

Apex=  131  )7220 

Average  systolic  blood-pressure     55  plus 

Apex,  79 ;  radial,  72 ;  deficit,  7. 
Radial   count, 
o 
44  44  x  110  =  4840 

64  —  44  =  20  x  IO°  =  2°oo 
72  —  64  =   8  x    9°  =    72° 
Apex  =79)7560 
Average  systolic  blood-pressure     95  plus 


Brachial 

pressure. 

100 

mm. 

Hg. 

90 

mm. 

80 

mm. 

70 

mm. 

60 

mm. 

50 

mm. 

B.S.,  May  11,  1910. 
Brachial  pressure. 

120  mm.  Hg. 

no  mm. 

100  mm. 
90  mm. 


ids  Auricular   Fibrillation 

The  estimation  of  blood-pressure  by  this  method  gives  us  a  sim- 
ple and  approximate  measure  of  this  factor  of  the  heart's  work. 
The  diastolic  pressure  may  be  roughly  determined  by  taking  a 
graphic  record  with  the  Erlanger  or  Uskoft"  instruments  and  noting 
the  pressure  at  which  the  average  excursion  of  the  pulse  waves  is 
maximal. 

Examined  by  this  method,  the  two  groups,  rheumatic  and  arterio- 
sclerotic, show  very  different  features. 

In  the  rheumatic-mitral  stenosis  group,  one  not  infrequently  sees 
an  average  systolic  blood-pressure  under  70  mm.  of  mercury ;  these 
are  usually  cases  with  rapid  rates  (over  140)  and  a  marked  degree 
of  cardiac  insufficiency.  With  improvement  the  blood-pressure 
rises  and  may  reach  120  mm.,  rarely  140. 

In  the  arteriosclerotic  group  with  fair  compensation  the  average 
systolic  blood-pressure  is  usually  160  mm.  or  over,  and  only  falls 
below  this  when  insufficiency  becomes  evident ;  in  this  group  when 
the  pressure,  estimated  in  the  above  manner,  falls  below  140  mm. 
myocardial  failure  is  very  threatening. 

The  irregular  activity  of  the  ventricle  is  unquestionably  the  re- 
sult of  the  peculiar  activity  of  the  auricles;  while  the  upper  cham- 
bers exhibit  no  gross  contractions  their  walls  show  an  incessant 
activity  composed  of  irregular  incoordinated  contractions  of  the 
muscle  fibers ;  impulses  from  the  auricles  are  showered  upon  the 
junctional  tissues  in  an  entirely  haphazard  fashion,  and  the  ventri- 
cles respond  in  utter  confusion  devoid  of  rhythm,  and  with  extreme 
variation  in  the  force  of  the  succession  beats. 

In  certain  cases  the  junctional  tissues  between  auricles  and  ven- 
tricles is  somewhat  damaged  so  that  conduction  between  the  cham- 
bers is  depressed  and  fewer  auricular  impulses  can  reach  the  ven- 
tricles (Figure  113)  ;  under  these  conditions  the  ventricular  rate  is 
not  excessive,  and  the  contractions  show  more  uniformity  in  force. 
Here  one  is  impressed  with  the  small  amount  of  disability  which 
results  from  the  fibrillating  auricle  ;  it  is  little  more  than  a  venous 
reservoir,  and  takes  little  part  in  moving  the  blood,  and  if  the  ir- 
regular impulses  which  are  initiated  in  its  wall  do  not  disturb  the 
ventricle  too  greatly,  the  circulation  is  maintained  with  a  reasonable 
degree  of  efficiency.  The  fibrillary  activity  may  be  continued  for 
years,  and  in  itself  is  not  at  all  incompatible  with  life  or  a  proper 
distribution  of  the  blood  to  the  various  organs. 


Auriculae    Fibrillai  con 


\<  ,< , 


Figure  127 

Auricular  fibrillation.     Fatient  C.  F.     Heart  very  rapid  and  irregular  (see  Figure  128). 


Figure  128 

Auricular  fibrillation,  patient  C.  F.,  taken  one  week  after  Figure  127.  The  auricles  are 
still  fibrillating,  but  the  heart  has  become  slow  under  appropriate  treatment.  This  is  a 
favorable   response  to  therapeutic  measures,   hence  in  this  case  the  prognosis  is  good. 


i7o  Auriculas  Fibrillation 


PROfiNO>TS 


This  depends  largely  on  two   factors;  first  the  integrity  of  the 

ventricular  muscle,  and  second  the  facility  with  which  the  shower 
of  impulses  coming  from  the  auricle  can  he  blocked.  With  a  weak, 
dilated  ventricle  showing  irritability  as  evidenced  by  frequent  ven- 
tricular extrasystoles  arising  from  points  in  the  ventricular  tissue 
other  than  the  A-V  bundle,  the  outlook  is  bad,  and  yet  under  skill- 
ful treatment  and  favorable  conditions,  such  a  heart  may  occasion- 
ally recover  a  considerable  degree  of  efficiency,  and  life  may  be 
prolonged  several  years.  Mere  dilatation  of  the  ventricle  if  other- 
wise healthy  need  cause  us  much  less  concern  if  careful  treatment 
is  instituted  soon  after  the  beginning  of  the  complete  irregularity; 
but  the  longer  the  period  between  the  onset  of  fibrillation  and  the 
employment  of  correct  therapeutic  measures,  the  more  difficult  is  it 
to  restore  the  damaged  ventricle.  In  the  majority  of  instances  digi- 
talis will  effectually  block  the  erratic  auricular  impulses,  and  give 
the  ventricle  the  lengthened  diastolic  period  so  necessary  for  its 
recuperation.  In  a  few  cases  digitalis  either  cannot  be  taken  in 
sufficient  amounts,  or  fails  to  obstruct  the  stimuli  from  the  upper 
chamber.  In  these  the  immediate  prospect  is  exceedingly  alarming. 
The  degree  of  the  response  of  the  heart  to  treatment  (see  Figures 
127  and  128),  and  the  amount  of  reserve  force  which  can  be  secured 
for  it,  are  our  best  indications  of  what  the  future  holds  in  store. 
Many  of  these  hearts  may  be  brought  to  a  fair  degree  of  efficiency, 
but  the  reserve  force  is  never  very  great,  and  neglect  of  treatment, 
or  over-exertion  will  almost  invariably  entail  an  attack  of  cardiac 
insufficiency.  Each  insult  of  this  kind  is  met  with  greater  difficulty 
and  with  each  attack  the  outlook  becomes  more  grave.  Auricular 
fibrillation  indicates  a  very  serious  myocardial  defect;  heart  failure 
may  be  postponed  for  many  years,  but  the  majority  succumb  within 
ten  years  of  its  onset. 

The  signs  which  point  to  a  favorable  prognosis  are : — 

1.  The  resumption  of  a  physiological  rhythm. 

2.  The  maintenance  of  a  rate  under  70. 

3.  The  absence  of  a  pulse  deficit. 

4.  The  absence  of  extrasystoles. 

5.  An  average  systolic  blood-pressure  of  over   no  in  the  rheu- 
matic group,  and  of  over  160  in  the  arteriosclerotic  group. 


Auricular   Fibrillation  171 

The  symptoms  which  make  the  outlook  grave  are : — 

1.  A  ventricular  rate  remaining  for  more  than  a  few  days  above 
130. 

2.  A  persistent  pulse  deficit  of  20  or  over. 

3.  The  occurrence  of  frequent  ventricular  extrasystoles. 

4.  A  falling  average  systolic  blood-pressure. 

5.  A  ventricular  rate  which  shows  wide  fluctuations  under  slight 
physical  or  emotional  stress. 

The  gravity  of  a  given  case  is  often  indicated  by  the  amount  of 
treatment  requisite  to  secure  a  slow  ventricular  rate  without  a  pulse 
deficit ;  some  cases  require  very  little  treatment,  and  in  these  the 
immediate  prognosis  is  good ;  others  yield  only  to  the  most  active 
therapeutic  measures  applied  over  a  very  long  period.  In  such  the 
danger  is  about  proportional  to  the  therapeutic  measures  found 
necessary. 

VENTRICULAR    FIBRILLATION 

Ventricular  fibrillation  has  been  recognized  as  a  terminal  event 
in  experiments  on  animals.  When  an  extreme  degree  of  ventricular 
irritability  is  produced  by  faradization  of  the  ventricle  (Levy)  or 
by  cutting  off  its  blood  supply*  the  coordinated  contractions  cease. 
These  are  succeeded  by  ineffectual  twitching  of  the  muscle  wall 
and  finally  by  diastolic  relaxation  with  fine  undulatory  movements 
of  the  surface,  and  in  a  few  seconds  the  animal  is  dead.  The  con- 
dition has  also  been  experimentally  produced  by  introducing  a  bubble 
of  air  into  the  coronary  artery. f  In  these  observations  the  ani- 
mals occasionally  recovered. 

In  man,  ventricular  fibrillation,  unless  of  only  momentary  dura- 
tion, is  incompatible  with  life.  Hoffmann|  has  reported,  with  elec- 
trocardiographic records,  a  condition  which  he  interpreted  as  a 
period  of  ventricular  fibrillation  occurring  at  the  end  of  a  paroxysm 
of  tachycardia ;  the  patient  ultimately  recovered.  As  far  as  I  know, 
this  is  the  only  instance  in  which  it  has  been  suggested  that  such 
an  outcome  is  possible,  and  it  is  not  altogether  clear  that  Hoff- 

*Lewis :  Mechanism  of  the  Heart  Beat,  London,   1911,  p.   160. 

fAlorat  and  Petzetakis :  Compt.  rend.  Soc.  de  Biol.,  1914.  lxxvii,  222,  377. 

JHoffmann:  Heart,  1911-12,  iii,  213. 


i7-  Ventricular  Fibrillation 

matin's  records  may  not  be  interpreted  a?  a  series  of  ventricular 
extrasystoles  arising   from  several  points  of  origin.     Ventricular 

fibrillation,  as  a  terminal  event,  has  been  studied  by  Robinson*  and 
by  1  talsey.f 

It  seeems  not  at  all  improbable,  as  McWilliams:;:  suggested,  that 
in  a  certain  number  of  cardiac  cases  Midden  death  may  be  due  t<> 
the  abrupt  onset  of  ventricular  fibrillation.  Levy§  has  shown  that 
the  administration  of  low  percentages  of  chloroform,  by  inhalation 
to  animals,  produces  a  high  degree  of  ventricular  irritability.  Under 
this  condition  small  reflex  sensory  stimulation  or  the  struggling 
of  the  animal  is  sufficient  to  induce  ventricular  fibrillation  and 
sudden  death.  If  adrenalin  was  given  intravenously  to  an  animal 
under  light  of  chloroform  anaesthesia,  ventricular  fibrillation  at  once 
ensued.  Levy  believes  that  the  cause  of  chloroform  death  in  man 
is  the  onset  of  ventricular  fibrillation  and  has  collected  from  the 
reports  of  sudden  death  under  chloroform  a  number  of  cases  which 
strongly  support  his  view. 

The  period  of  danger  is  at  the  time  the  patient  is  getting  very 
little  chloroform,  at  the  beginning  of  its  administration  or  when 
it  is  given  intermittently.  To  avoid  this  danger,  all  nervous  ex- 
citement for  the  patient  must  be  excluded.  No  manipulations  must 
be  attempted  until  he  is  well  under  the  anaesthesia.  The  chloro- 
form must  be  given  continuously  and  in  considerable  amounts. 
Adrenalin  should  not  be  used  in  conjunction  with  chloroform. 

♦Jour.   Exp.   Med.,   1912,   xvi,  291. 
^Tleart :   1915,  vi,  67. 
tBrit  Med.  Jour.,  1889,  i,  6. 
§Heart,  1912-13,  iv,  319. 


CflAITKK   XI  f 
Auricular  Flutter,  Tachycardia  and  Fibrillation 

These  forms  of  arrhythmia  have  been  discussed  in  separate  chap- 
ters, but  it  may  not  be  amiss  to  say  a  few  words  about  their 
close  association  and  to  examine  the  slight  modifications  in  mech- 
anism which  may  lead  to  the  transition  of  one  into  another. 

In  1887,  McWilliams,*  in  investigating  the  activities  of  the  dog's 
heart  under  different  experimental  conditions,  called  attention  to 
the  variation  in  the  nature  of  the  response  of  the  auricles  to  faradic 
currents  of  greater  and  less  intensities.  lie  found  that  (i)  when 
he  stimulated  the  auricular  tissues  with  a  weak  faradic  current 
the  auricles  contracted  at  a  very  rapid  rate  in  perfect  rhythm.  If, 
however,  the  strength  of  the  stimulating  current  was  increased, 
(2)  the  auricles  ceased  to  contract  as  a  whole,  the  walls  relaxed 
and  assumed  the  diastolic  position,  but  the  muscle  movements  did 
not  stop ;  the  whole  surface  of  the  auricles  took  on  an  undulatory, 
incoordinated  activity  with  irregular  twitching,  but  with  no  actual 
systole  of  the  upper  chamber.  Finally,  (3)  when  stimu- 
lating current  was  withdrawn,  the  auricles  resumed  their  accustomed 
deliberate  coordinated  contractions.  In  the  first  instance,  the  ven- 
tricles responded  rhythmically,  in  response  to  each  auricular  con- 
traction or  more  often  to  every  other  auricular  impulse.  Under 
the  conditions  of  the  second  stage  of  the  experiment,  the  ven- 
tricles responded  in  a  haphazard  fashion  with  complete  irregularity. 
Finally,  when  the  auricles  recovered  their  accustomed  activity,  the 
ventricles  responded  in  a  normal  manner. 

Since  these  earlier  observations,  these  different  activities  have 
been  elaborately  studied  and  are  now  recognized  as  "auricular 
flutter,"  "paroxysmal  auricular  tachycardia"  and  "auricular  fibril- 
lation." McWilliams'  observations  have  been  verified  by  a  num- 
ber of  other  investigators.  Hirschfelderf  was  able  to  produce  at 
will  "auricular  tachycardia"  or  "auricular  fibrillation,"  according 
to  the  strength  of  the  faradizing  current.     The  same  phenomena 

*Jour.  Physiol.,  1887,  viii,  296. 

fBull.  Johns  Hopkins  Hosp.,  1908,  xix,  222- 

173 


174    Auriculas  Flutter,  Tachycardia  and  Fibrillation 

were  observed  by  Robinson,*  who  found,  further,  that  if  the  right 
vagus  was  stimulated  during  a  period  of  experimental  tachycardia 

there  was  a  transition  to  auricular  fibrillation,  while  stimulation  of 
the  left  vagus  did  not  inhibit  the  auricular  tachycardia,  but  blocked 

a  portion  of  these  impulses  so  that  the  ventricle  failed  to  respond 
to  every   auricular   contraction,      lie   helieves   that    in   the   experi- 


FlGURE    129 


Figure  130 


mental  animal  faradization  of  the  auricles  produces  a  mixed  effect 
which  is  a  comhination  of  "flutter"  and  "fibrillation." 

If  one  examines  a  number  of  electrocardiograms  taken  from  a 
series  of  patients  with  complete  irregularity,  one  is  at  once  impressed 
with  the  great  variety  in  the  size  and  the  rhythmicity  of  the  waves 
representing  the  auricular  activity  In  one  they  are  so  small  as 
to  be  almost  imperceptible  and  show  no  tendency  to  rhythmicity; 

*Jour.  Exp.   Med.,   1913,  xviii,  704. 


Auricular  Flutter,  Tachycardia  and  Fibrillation     175 


Figure  131 


f 

r^ 

FFf=^ 

HSBE 

prr 

prrr 

m i' 

n=rr 

P^T— 

pzr 

CT= 

, '   .'i      ,     '    ■   ; .  'in 

r 

-_ — 

^ft 

±rrr 

#3= 

■  'i 

^E 

r— -f-          ■      1  "~~j     ^zj 

IS 

i^j^Ji 

1      i  '    :    ■■! 

I 

i    :  ■     -:      .     'i 

Figure  132 


Figure  133 


Figures  129-133. — Records  from  five  different  cases  of  complete  irregularity.  Arranged 
to  show  gradations  in  the  size  and  rhythmicity  of  the  undulations  representing  auricular 
activity   and  the  ventricular  response. 


i7''    Auricular  Flutter,  Tachycardia  and  Fibrillation 

in  another  these  wave?  may  he  very  large  and  reenr  at  quite  defi- 
nite intervals. 

A  series  of  records  of  this  kind  is  shown  in  Figures  l-'o,  130, 
131,  [32  and  [33.  They  have  been  arranged  to  show  the  grada- 
tions that  are  seen  in  a  collection  of  such  curves.  They  vary 
from  small  irregular  deflections  to  those  of  considerable  size  and 
degree  oi  rhythmicity.  <  me  may  say  that,  as  a  rule,  as  the  auricu- 
lar waves  increase  in  size,  the  tendency  is  for  them  to  become  rhyth- 
mic, and  also  for  the  ventricle  to  respond  to  the  auricular  impulses 
at  more  regular  intervals. 

When  one  examines  the  fust  record  (  Figure  129)  of  this  series, 
it  conforms  quite  definitely  to  our  conception  of  the  classical  pic- 
ture of  auricular  fibrillation  with  the  minute,  very  irregular  fibril- 
lary manifestations  and  the  complete  irregularity  in  ventricular 
response. 

In  the  last  record  of  the  series  (Figure  133)  the  undulatory 
waves  are  very  much  larger  and  quite  rhythmic.  The  ventricular 
response  is  irregular,  but  not  more  so  than  might  be  seen  in  a 
case  of  "auricular  flutter"  with  a  block  of  varying  degree.  An 
inspection  of  the  intervening  records  show  gradations  which  sug- 
gest that,  under  various  pathological  conditions  which  are  not  under- 
stood, and  at  present  cannot  be  differentiated,  there  may  be  all 
grades  of  auricular  activity,  such  as  the  incoordinated  contraction 
of  individual  muscle  fibers,  contractions  in  which  a  group  of  fibers 
are  coordinated  and  contractions  resulting  from  a  coordinated  ac- 
tivity of  the  entire  musculature. 

The  close  relationship  of  "auricular  flutter"  and  "auricular  fibril- 
lation" may  be  further  inferred  from  the  ease  with  which,  in  the 
individual  patient,  the  activity  may  change  from  one  form  to  the 
other.  Instances  of  this  transition  have  been  illustrated  in  the 
chapter  on  "auricular  flutter"  (Figures  92,  93,  96,  97  and  98). 

It  has  been  suggested  that  in  "auricular  flutter"  the  auricular 
contractions  arise  not  from  the  normal  pacemaker,  the  sinus  node, 
but  from  some  point  of  abnormal  irritability  in  the  auricular  wall ; 
in  other  words,  that  they  are  true  auricular  extrasystoles.  If  such 
is  the  case,  it  would  bring  our  ideas  of  the  mechanisms  of  "auric- 
ular flutter"  and  "auricular  tachycardia"  into  a  very  close  relation- 
ship.    Such  a  conception  is  borne  out  by  a  study  of  the  records 


Auricular  Flutter,  Tachycardia  and  Fibrillation     177 


p    p  p  p  p 


^.^■A^&flSMMlMlrif&f&ftf*! 


Figure  134 

Record  of  T.  K.  showing  transition  from  complete  irregularity  Cauricular  fibrillation) 
to  rhythmic  auricular  flutter  with  a  2  to  1  ventricular  response  fl's=  120,  As  =  340; 
and   the   return   to  ci  mplete   irregularity. 


Figure  135 

Record  of  T.   K.  taken  a  few  minutes  after  Figure   134,  showing  rhythmic  tachycardia 
(Vs  =  240).      The    ventricle    responds    to    each   auricular   impulse. 


Figure  136 

Transition    from   auricular   flutter    with    irregular   response    to    rhythmic   tachycardia 
[I  s  =  1S0.) 


178    Auriculas  Flutter,  Tachycardia  and  Fibrillation 

(Figures  T34,  F35  and  13;  I  from  a  patient  who  was  under  obser- 
vation For  a  period  of  less  than  two  hours,  during  which  these 
curves  and  a  number  of  others  were  secured.  The  beginning  and 
the  end  of  the  electrocardiogram  (Figure  134)  ran  lie  interpreted 
as  auricular  fibrillation.  In  the  center  of  this  record  there  is  a 
rhythmic  period  during  which  there  appears  an  auricular  flutter, 
with  a  ventricular  response,  to  every  other  auricular  impulse.  A 
few  minutes  later  this  passed  into  a  period  of  rhythmic  auricular 
tachycardia  (Figure  135).  during  which  the  ventricular  rate  is  jusl 
double  the  rate  of  the  rhythmic  period  of  Figure  134.  It  seems 
evident  that  the  auricle  is  still  in  flutter  and  that  now  the  ven- 
tricle is  responding  to  each  auricular  contraction. 

Figure  [37  is  a  polygraph  secured  from  the  same  patient  a  few 
minutes  later  and  shows  the  transition  from  a  period  of  flutter, 
with,  irregular  ventricular  response,  to  one  of  rhythmic  tachycardia. 
The  electrocardiogram  of  another  patient  showing  a  transition 
from  an  auricular  flutter,  with  an  irregular  ventricular  response, 
to  a  typical  paroxysm  of  auricular  tachycardia,  terminating  again 
in  auricular  flutter,  is  presented  in  Figure  [36.  This  patient  was 
under  observation  for  many  weeks  and  her  heart  recovered  a  nor- 
mal rhythm.  During  none  of  this  time  was  it  possible  to  obtain 
any  conclusive  evidence  of  auricular  fibrillation. 

Such  observations  suggest  that  there  is  a  very  close  relationship 
between  these  types  of  abnormal  auricular  activity. 


Auricular  Flutter,  Tachycardia  and  Fibrillation     179 


Jugular 


Brachial 


o.z  second 


Figure  137 

Polygraph   of  T.   K.  taken  immediately  after  Figures  134  and   135,  showing  transition 
from  auricular  flutter  with  irregular  response  to  rhythmic  tachycardia. 


CHAPTER  XU1 

Alternation 

The  palpation  of  the  arterial  pulse  often  presents  to  the  clinician 
a  series  of  waves  which  alternately  vary  in  size.  The  waves  recur 
with  perfect  rhythmicity  for  considerable  periods.  There  is  a  large 
wave,  then  a  small  wave,  another  large  wave  Eollowed  by  a  small 

wave,  and  so  on  for  hours  or  days.  This  condition  is  known  as 
alternation  of  the  pulse.  The  term  alternation  is  not  confined  to 
this  pulse  phenomenon,  but  is  also  used  to  designate  a  similar  al- 
ternating activity  of  the  heart  and  of  the  jugular  veins. 

The  term  alternation  requires  further  definition  than  the  mere 
statement  that  large  and  small  pulse  waves  follow  one  another. 
Alternation  should  he  reserved  for  that  activity  of  the  heart  in 
which  forcihle  and  weak  contractions  succeed  one  another  rhyth- 
mically, and  in  which  the  interval  between  the  large  and  small 
beats  is  equal  to  or  greater  than  the  interval  between  the  small 
and  the  large  beats.  It  is  to  he  distinguished  from  the  pulsus 
bigeminus,  in  which  every  other  cardiac  contraction  is  an  extra- 
systole,  and  also  from  the  pseudo-alternans  detected  in  both  veins 
and  arteries,  which  is  directly  dependent  on  respiratory  movements. 

EXPERIMENTAL    PRODUCTION    AND    MECHANISM 

Alternation  has  been  studied  extensively  in  both  cold-  and  warm- 
blooded animals.  In  the  course  of  experimental  studies  of  various 
kinds,  it  occurs  spontaneously  and  has  also  been  produced  by  utiliz- 
ing various  poisonous  substances.  It  has  been  seen  in  the  isolated 
and  perfused  heart  and  in  the  heart  exposed  by  removing  a  por- 
tion of  the  chest  wall.  In  the  suspended  heart,  it  has  been  pro- 
voked by  withdrawing  the  supply  of  Ringer's  or  Locke's  solution, 
by  the  substitution  of  carbon  dioxid  for  the  oxygen,  by  the  intro- 
duction of  hemolytic  serum,  etc.,  etc.  This  activity  has  been  in- 
duced in  the  heart  in  situ  by  the  introduction  of  digitalis  and  aconi- 
tine  (Cushny)  and  antiarin  (Straub)  and  glyoxylic  acid  (Ilerirg, 
Rihl,  Kahn  and  others).     Alternation  may  appear  during  the  ap- 

180 


Alternation  i  Hi 

plication  of  electrical  stimulation  to  the  myocardium  rind  while  the 
extracardial  nerves  arc  being  manipulated. 
The  difference  in  the  successive  waves  may  be  in  their  contour, 

rather   than   their   size.      Their   dissimilarity    is    practically    alv. 
demonstrable  by  a  time  pressure  curve,  but  the  electrocardiogram 

furnishes  evidence  of  alternation  only  on  very  infrequent  occa- 
sions. When  this  is  present,  it  consists  in  an  alternating  height 
of  the  R  wave,  more  rarely  in  a  change  in  the  elevation  of  the  / 
wave. 

The  mechanism  of  alternation  is  still  a  matter  of  considerable 
speculation.  The  majority  of  investigators  ascrihe  this  abnormal 
function  to  a  defect  in  the  contractility  of  the  heart.  It  has  been 
supposed  that  under  pathological  conditions  different  muscular 
fibers  have  different  refractory  periods,  so  that  at  one  time  all 
the  fibers  are  active,  at  another  only  a  portion  take  part  in  the 
contraction  (Wenckebach,  Mines).  A  view  that  has  received  con- 
siderable support  is  that  the  cardiac  fibers  differ  in  their  excitability 
and,  hence,  respond  to  stimuli  at  uneven  intervals  (Gaskell,  Kron- 
ecker).  The  abnormal  activity  has  also  been  thought  to  be  de- 
pendent on  a  defect  in  conductivity  (Engelmann,  Muskens).  It 
is  clear  that  as  yet  the  evidence  is  not  conclusive  in  regard  to  the 
fundamental  properties  of  cardiac  tissues  which  are  at  fault  in 
the  production  of  this  irregularity.  On  clinical  grounds,  it  seems 
to  me  that  in  alternation  we  are  dealing  with  a  phenomenon  which 
may  be  produced  by  a  defect  of  contractility  at  one  time  and  at 
another  time  by  a  defect  of  conductivity.  I  believe  that  further 
study  will  permit  us  to  segregate  our  cases  of  alternans  into  groups, 
each  of  which  may  be  shown  to  be  due  to  a  different  defect. 

A  presentation  of  the  various  theories  of  alternation  and  a  crit- 
ical review  have  been  published  by  Gravier*  in  a  recent  thesis. 

PATHOLOGY 

There  are  reported  in  the  literature  about  twenty  autopsies  in 
subjects  in  whom  alternation  of  the  heart  has  been  a  prominent 
feature  and  in  whom  this  arrhythmia  has  been  verified  by  graphic 
methods.  Some  of  these  reports  are  not  at  all  complete;  others 
give  in  considerable  detail  the  histological  findings  obtained  from 

*L'Alternance  du  coeur,  Paris,  1914. 


1 82  Alternation 

a  very  exhaustive  Study  of  the  cardiac  muscle.  Practically  all  of 
the  hearts  thus  examined  have  presented  anatomical  lesions  of 
greater  or  less  extent.  'There  is  usually  an  hypertrophy,  particu- 
larly of  the  left  ventricle,  with  some  degree  of  degeneration  of 
the  muscle  fibers  ^h\^  to  a  perivascular  sclerosis.  These  lesions 
are,  as  a  ride,  quite  extensive  and  are  not  limited  to  any  special 
part  of  the  cardiac  tissues.  In  some,  the  lesions  have  involved 
portions  of  the  conduction  system,  but  this  finding  is  not  at  all 
constant.  We  may  conclude  that,  as  yet,  we  have  no  evidence 
which  permits  us  to  assign  this  functional  disturbance  to  a  special 
anatomical   lesion. 

The  ease  with  which  alternation  may  he  provoked  in  the  normal 
cardiac  tissue  of  experimental  animals  by  the  administration  <>i 
toxic  substances,  such  as  aconitine,  digitalis,  glyoxylic  acid,  stro- 
phanthin,  veratrin,  etc.,  has  suggested  that  this  functional  abnor- 
mality may  be  the  result  of  a  cell  intoxication.  Digitalis  must  al- 
ways be  thought  of  as  a  possible  factor,  but  one  frequently  sees 
alternation  in  patients  who  have  never  had  this  drug.  Hering  has 
described  alternation  in  a  man  poisoned  with  strychnine.  As  alter- 
nation is  not  an  uncommon  accompaniment  of  advanced  nephritis, 
it  has  been  suggested  that  it  is  a  manifestation  of  uremic  poisoning. 

The  remarkable  properties  of  glyoxylic  acid  in  producing  alter- 
nation experimentally,  and  the  fact  that  this  acid  may  be  a  product 
of  abnormal  metabolism,  gives  us  a  hint  of  another  possible  source 
of  an  auto-intoxicant. 

ETIOLOGY 

Our  ideas  of  the  frequency  of  the  occurrence  of  the  various 
arrhythmias  of  the  heart  is  changing  very  greatly.  The  routine 
painstaking  examination  of  large  numbers  of  patients  has  demon- 
strated that  irregularities  which  were  once  believed  to  be  very 
exceptional  are  in  reality  not  uncommon.  This,  for  example,  has 
been  our  experience  with  "auricular  flutter."  At  one  time  this  was 
regarded  as  a  very  unique  finding ;  today  it  is  not  unusual  to  have 
more  than  one  such  case  always  under  observation.  A  similar 
transition  has  occurred  in  our  notions  of  the  frequency  of  alter- 
nation. Xot  long  ago  it  was  thought  to  be  rather  a  rare  symp- 
tom;  to-day,  according  to  the  statistics  of  some  observers,  it  ranks 


Alternation 


i 


Hr.v  hial 


0.2   second 


Figure  138 

Alternation   in  brachial  and  jugular.   Note   variation   in   amplitude   of   a   waves.     Taken 
from   same   case   as    Figure    139,   only   a   few   minutes   separate   the   two   records. 


^V    J'<'\J 


a  Mttk-JX—  _rfWL_L  J^JLti   rfMn  t\        ttk  tk       ^JK^k^  -AA.  ^ 


6.2  stcondi 


, *■     :.. 


Jujju!ar 


Figure  139 

Jugular  and  electrocardiogram  taken  simultaneously.  By  palpation  the  radial  was 
alternating  at  this  time.  There  is  no  evidence  of  alternation  in  the  electrocardiogram. 
Same  case  as  Figure  138. 


1S4  Alternation 

in  frequency  only  second  to  the  extrasystole.  In  a  recent  study  of 
three  hundred  cardiac  cases.  White,*  during  a  period  of  eight 
months,  discovered  no  less  than  seventy-one  cases  of  .alternation, 
lie  found  this  irregularity  in  thirty-three  per  cent,  of  all  the  cases 
showing  any  degree  of  cardiac  decompensation  in  which  he  se- 
cured graphic  records. 

Alternation  is  more  frequent  in  the  old  than  in  the  young,  but 
has  been  observed  in  all  ages  from  fifteen  to  seventy-five  years. 
It  is  a  common  manifestation  in  myocarditis  with  hypertension. 
In  my  own  experience  it  has  most  often  been  seen  in  cases  of 
chronic  nephritis  or  general  arteriosclerosis,  which  have  recently 
been  admitted  to  the  hospital  wards. 

Alternation  is  rather  uncommon  in  the  course  of  the  acute  in- 
fections, but  it  has  been  noted  in  pneumonia,  diphtheria,  typhoid 
fever  and  rheumatism.  It  is  seen  in  cases  of  chronic  valvular  dis- 
ease and  pericarditis  which  are  of  rheumatic  origin. 

Alternation  has  been  observed  in  acute  dilatation  (  Mackenzie) 
in  a  case  showing  myocardial  infarcts  (Gallavardin)  and  in  strych- 
nin poisoning   (Hering). 

White  obtained  a  positive  Wassermann  reaction  in  fifteen  per 
cent,  of  his  cases,  and  a  history  of  overindulgence  in  alcohol, 
tobacco  and  tea  was  notable.  In  an  analysis  of  forty-five  cases 
of  alternation,  Windlef  observed  that  the  associated  conditions 
presented  the  following  order  of  frequency:  (i)  Arterial  and  myo- 
cardial disease;  (2)  chronic  heart  disease  due  to  rheumatism;  (3) 
pneumonia,   and    (4)    acute   rheumatic   carditis. 

In  a  considerable  number  of  patients  showing  alternans,  this 
is  by  no  means  the  only  evidence  of  myocardial  defect.  In  asso- 
ciation are  found  many  other  types  of  cardiac  arrhythmia.  A  lat- 
ent alternation  often  becomes  evident  when  the  heart  rate  is  accel- 
erated, hence  alternation  is  a  very  common  accompaniment  of  very 
rapid  hearts,  particularly  those  showing  paroxysmal  tachycardia 
(Figures  140,  150  and  151).  Many  also  present  signs  of  imper- 
fect conduction.  Alternation  is  quite  common  in  cases  of  "auric- 
ular flutter"  (see  Figure  [46)  and  this  is  not  surprising  when  we 
recall  that   in   the  latter  condition  conduction  defects  and  tachy- 

♦Amer.  Jour.  Med.  Sc,  1915,  cl,  82. 
■rQiiart.  Jour.   Med.,    1912,  vi,  453. 


Alternation 


Jugular 


Apex 


Radial 


0.2   second 


Figure  140 

Alternation    of   apex,    radial   and   jugular.      Tachycardia    rate    200. 


i86  Alternation 

cardia  are  very  often  in  evidence.  The  association  of  extrasystoles 
is  a  Frequent  finding  and  an  alternation  which  may  have  been  quite 
unnoticed  may  become  very  pronounced  in  the  cycles  immediately 
following  an  extrasystole.  This  is  so  common  that  it  has  been 
given  a  special  name,  the  "post-extrasystolic  alternans." 

It  seems  to  me  that  the  evidence  is  very  suggestive  that  in  cer- 
tain cases  of  alternans  the  exciting  cause  of  this  irregularity  is 
really  a  lack  of  proper  nutrition  of  the  myocardial  calls.  Under 
conditions  of  stress,  the  tissues  have  too  little  oxygen  or  there  is 
an  accumulation  of  COa  or  possibly  other  toxins  which  may  be 
the    intermediary   products   of   abnormal    metabolism. 

[DENTIFICATK  IN 

The  more  pronounced  types  of  alternation  may  be  detected  by 
palpation  of  one  of  the  peripheral  arteries.  This  is  naturally  more 
easily  accomplished  when  the  large  and  small  arterial  waves  show 
a  considerable  difference  in  the  systolic  blood  pressures.  This  dif- 
ference usually  does  not  exceed  ten  millimeters  of  mercury,  but 
occasionally  may  be  as  much  as  twenty  millimeters  (Rihl).  With 
the  smaller  variations  in  pressure  this  important  type  of  irregularity 
often  passes  unobserved,  but  if  one  is  constantly  on  the  outlook 
for  it  in  cases  in  which  it  may  be  suspected,  such  as  nephritics, 
general  arteriosclerotics,  etc.,  it  will  be  discovered  with  consid- 
erable frequency.  There  are  several  simple  means  which  may  aid 
in  the  detection.  Palpation  of  the  pulse  should  always  be  made 
with  the  tips  of  several  fingers,  not  with  one  ringer  alone,  and 
while  one  is  making  the  observation  the  pressure  exerted  on  the 
arterial  wall  should  be  changed,  as  this  often  accentuates  the  dif- 
ferences in  the  size  of  the  waves.  A  latent  alternans  may  fre- 
quently be  made  more  evident  by  partly  occluding  the  artery  above 
the  palpating  fingers.  This  may  be  accomplished  by  exerting  pres- 
sure on  the  brachial  artery  by  means  of  the  cuff  of  a  sphygmonan- 
ometer  or  by  digital  pressure  of  the  axillary  artery  (Gallavardin  and 
Gravier).  The  pressure  thus  applied  should  be  varied  in  amounts, 
as  it  is  difficult  to  predict  in  advance  what  degree  of  pressure 
will  best  accentuate  the  pulse  differences.  A  little  exertion  to  in- 
crease the  rate  of  the  heart  may  be  of  service  in  rendering  the 
alternation  more  evident. 


Ar.TKKNATION 


187 


Figure  141 

Radial  tracing   showing  alternation   and    probably   one   extrasystole. 


Figure  142 

Radial  tracing  showing  alternation.  While  this  record  was  being  taken  a  pressure 
of  85  mm.Hg.  was  applied  to  the  brachial  artery  through  a  sphygmomanometer  cuff  in 
order  to  bring  out  the  differences  in  amplitude  of  the  successive  waves. 


i88  Alternation 

In  palpation  the  attention  must  be  directed  not  only  to  the  varia- 
tion in  amplitude  of  the  successive  waves,  but  also  to  their  spacing; 
if  the  impression  is  obtained  that  the  interval  between  the  small 
and  succeeding  large  wave  is  greater  than  the  interval  between  the 
large  wave  and  succeeding  small  wave,  the  irregularity  is  more 
probably  an  extrasystolic  "bigeminus"  than  an  alternation.  This 
is  the  irregularity  which  has  most  often  been  confused  with 
alternation. 

Palpation  of  the  precordial  region  may  give  evidence  similar  to 
that  secured  from  palpation  of  the  peripheral  arteries,  but  this 
is  usually  an  uncertain  aid.  Auscultation  of  the  heart  rarely  re- 
veals a  difference  in  the  intensity  of  the  sounds  of  the  strong  and 
weak  beats.  When  murmurs  are  present,  they  occasionally  vary 
in  intensity,  but  a  change  in  heart  sounds  normal  and  pathological 
are  far  more  characteristic  of  the  extrasystolic  irregularities  and 
auricular  fibrillation  than  they  arc  of  alternation. 

In  rare  cases  of  alternation,  inspection  of  the  venous  pulse  shows 
a  great  variation  in  amplitude  of  every  other  cycle,  thus  giving  us 
a  clue  to  the  type  of  the  irregularity  (see  Figure  140). 

Unless  instrumental  means  are  employed  as  a  routine,  many 
cases  of  alternation  will  escape  recognition.  Painstaking  observa- 
tions with  the  sphygmograph  are  our  only  sure  means  of  detect- 
ing pulsus  alternans  in  a  very  large  number  of  instances.  These 
records,  taken  under  the  various  conditions  outlined  in  discussing 
palpation  of  the  pulse,  present  to  us  the  minute  variations  in  the 
amplitude  and  spacing  of  the  succession  waves,  which  will  often 
escape  even  the  highly  cultivated  tactile  sense  of  the  expert. 

Typical  sphygmograms  are  presented  in  Figures  141  and  142. 
In  these  records  the  difference  in  the  amplitude  of  the  alternate 
waves  and  their  rhythmic  spacing  is  well  illustrated.  Figure  141 
is  a  radial  tracing  from  a  case  in  which  the  alternation  was  quite 
evident  from  palpation  of  the  pulse.  Figure  142,  also  taken  from 
the  radial  pulse,  was  only  brought  out  distinctly  when  a  brachial 
cuff,  with  pressure  85  mm.  Hg.,  was  applied.  Some  cases  of  al- 
ternans have  been  published  with  graphic  records  in  which  the 
successive  waves  differ  in  duration  rather  than  amplitude.* 

Graphic  records  of  the  apex  beat  are,  as  a  rule,  rather  unsat- 

*Gravicr,  loc.  cit.,  p.  44. 


Alternation 


,89 


1 


Apex 


Radial 


0.2   second 


Figure  143 

Polygram  showing  alternation  in  radial  and  apex. 


iyo  Alternation 

is  factory  in  detecting  this  condition.  It  is,  however,  fairly  well 
shown  in  Figures  140  and  143.  In  these  records  the  alternation 
in  the  radial  is  quite  evident.     The  alternation  in  the  apex  activity 

is  indicated  by  the  notching  of  every  other  wave  of  the  cardio- 
gram. 1  [ering  has  pointed  out  that  tracing,  taken  in  the  precordial 
region  near  the  base  of  the  heart,  sometimes  shows  an  alternation 
when  it   is  absent  in  records  taken  near  the  apex. 

The  respiratory  movements  of  the  chest  are  prone  to  affect  the 
contour  of  the  waves  of  the  cardiogram,  but  in  these  records  the 
evidence  is  quite  conclusive  that  the  variation  in  the  waves  is 
quite  independent  of  the  breathing.  It  may  be  noted  in  this  con- 
nection that  in  cases  with  a  slow  pulse  and  rapid  respiration,  when 
the  pulse  rate  is  approximately  double  that  of  the  respiration,  the 
peripheral  arteries  may  show  a  difference  in  the  size  of  the  suc- 
cessive beats  which  simulates  alternation.  The  pulse  wave  coin- 
cident with  inspiration  is  smaller  than  that  corresponding  to  ex- 
piration. This  pseudo-alternans  is  easily  differentiated  by  having 
the  patient  hold  his  breath  when  the  amplitude  of  the  pulse  waves 
at  once  becomes  uniform. 

Alternation  may  or  may  not  appear  in  the  venous  tracings  and 
may  assume  several  forms.  There  may  be  alternation  of  the  c 
waves,  of  the  v  waves  or  of  the  a  waves. 

In  Figure  144  is  shown  a  well-marked  alternation  in  the  arterial 
record,  but  no  evidence  of  this  irregularity  in  the  jugular.  Respira- 
tory movements  are  much  more  likely  to  distort  the  phlcbogram, 
hence  in  cases  of  doubt  it  is  always  a  wise  precaution  to  secure 
the  record  during  a  period  of  suspended  breathing. 

Alternation  in  the  c  wave  is  quite  evident  in  Figure  145.  Here 
the  large  c  wave  corresponds  to  the  large  wave  of  the  brachial, 
which  is  quite  what  one  would  expect.  Occasionally  one  sees  cases 
in  which  the  small  c  wave  corresponds  to  the  large  peripheral  ar- 
terial wave.     The  explanation  of  this  phenomenon  is  difficult. 

Alternation  of  the  auricle  is  seen  in  experimental  work  and  may 
be  diagnosed  in  the  clinic  by  an  alternating  amplitude  in  the  a 
wave  of  the  jugular  tracing.     Such  a  record  is  exhibited  in  Figure 

138. 

On  the  whole,  evidence  of  venous  alternation  is  rather  rare  and 
its   significance  has  not  been   carefully  studied. 


Alternation 


191 


Jugular 


Brachial 


0.2   second 


Figure  144 

Alternation  of  brachial,  no  alternation  in  jugular. 


Jugular 


Brachial 


0.2   second 


Figure  145 

Alternation  of  brachial   and  of  c  wave  of  tracing  taken  from  above  the  clavicle. 


iy_>  Alternation 

A  very  beautiful  exhibition  of  alternation  involving  radial  apex 
and  jugular  curves,  is  shown  in  Figure  140.  This  record  was  se- 
cured from  a  man  suffering  from  advanced  myocardial  disease 
Several  months  before  his  death.  This  curve  was  taken  during  an 
attack  of  paroxysmal  tachycardia,  during  which  the  rate  was  200 
per  minute.  The  phlebogram  is  difficult  to  analyze,  since  the  a,  C 
and  ?'  waves  are  fused  together.  At  other  times  there  was  also 
evidence  oi  a  prolonged  a-C  interval,  so  this  element  also  compli- 
cates the  analysis.  It  would  seem  that  there  is  in  this  case  alterna- 
tion of  the  X'  wave,  due  to  alternating  ventricular  activity,  which  is 
very  prominent  on  account  of  an  insufficient  tricuspid  valve.  There 
also  would  appear  to  be  an  alternation  of  the  auricle,  as  evidenced 
by  the  differences  in  amplitude  of  the  a  waves,  but  this  is  less 
certain. 

The  electrocardiogram  rarely  shows  evidence  of  alternation.  The 
differences  in  amplitude  of  the  waves  of  the  peripheral  arteries 
may  be  quite  evident,  and  yet  the  successive  cycles  of  the  heart, 
as  portraved  by  the  galvanometric  curves,  may  present  great  uni- 
formity (see  Figures  139,  146,  148  and  149).  In  Figure  146  are 
presented  simultaneous  curves  of  a  radial  pulse  and  the  electro- 
cardiogram. The  latter  record  shows  that  we  are  dealing  with  a 
case  of  auricular  flutter  with  an  irregular  ventricular  response.  The 
radial  waves  distinctly  alternate  in  amplitude,  but  it  would  seem 
that  their  rhythmic  spacing  is  due  to  a  delay  in  the  transmission 
of  the  smaller  waves  to  the  periphery,  rather  than  to  a  true  alter- 
nating cardiac  activity. 

Figure  147  was  secured  from  an  old  gentleman  with  cardiac  de- 
compensation and  a  pulse  which,  on  palpation,  closely  simulated  an 
alternans.  The  combined  record  shows  that  the  irregularity  is 
really  not  due  to  alternation,  but  to  ventricular  {Vx)  and  auricu- 
lar (Ax)  extrasystoles. 

A  true  alternans,  which  is  complicated  by  a  single  premature 
beat,  is  presented  in  Figure  148.  The  abnormal  form  of  the  usual 
ventricular  complex  suggests  a  lesion  of  one  branch  of  the  A-V 
bundle. 

Rarelv  one  obtains  electrocardiographic  evidence  of  alternation 
of  the  heart.  This  may  consist  in  varying  amplitudes  of  the  R 
or  of  the  T  waves.     Two  such  curves  are  shown  in  Figures  150 


Alternation 


"J3 


Radial 


FlGXJRE    146 

Radial    showing    alternation.       The    electrocardiogram    shows    auricular    flutter    with 
irregular    ventricular    response. 


~  *    Brachial 


Figure  147 

Pseudo-alternation     of     brachial     due     to     ventricular     (Vx)     and     auricular     (Ax) 
extrasystoles. 


194 


Alternation 


and  151.  Figure  [50  was  from  a  woman  suffering  from  parox- 
ysmal tachycardia  ;  between  the  attacks  neither  radial  tracings  nor 
the  galvanometer  showed  evidence  <it'  alternation.  Soon  after  the 
onset  of  the  paroxysm,  the  alternation  could  be  detected  both  in 

the  peripheral  arteries  and  in  the  electrocardiogram.  The  elec- 
trocardiographic record  shows  a  well-marked  variation  in  ampli- 
tudes of  the  R  waves.  Figure  151  was  secured  from  a  man  who 
at  various  times  gave  electrocardiographic  evidence  of  defective 
conduction,  extrasystoles,  etc.  He  had  frequent  short  paroxysms 
of  ventricular  tachycardia,  never  exceeding  three  minutes  in  dura- 
tion. In  some  of  these  attacks  the  alternation  in  the  ventricular 
complexes  appeared,  as  shown  in  the  cut.  He  left  the  hospital 
with  a  fairly  regular,  but  evidently  much  diseased,  heart.  Unfor- 
tunately, he  removed  to  another  city,  and  we  have  been  unahle 
to  secure  information   in   regard  to  the  outcome. 

CLINICAL  FEATURES 

I  have  never  seen  a  patient  who  was  conscious  of  the  alternation 
of  his  pulse.  It  is  the  other  commonly  associated  symptoms  which 
bring  him  to  the  physician.  There  is  almost  always  some  dyspnoea ; 
this  may  be  of  mild  degree  or  of  the  most  extreme  type.  Many  of 
them  have  Cheyne-Stokes  breathing,  some  have  nocturnal  dyspnoea, 
which  occurs  in  paroxysms  and  wakes  them  from  their  sleep.  Pa- 
tients with  alternans  are  frequently  the  subjects  of  anginal  pain. 
It  is  quite  clear  that  the  alternation  is  merely  one  of  the  mani- 
festations of  a  failing  heart,  but  one  that  is  of  considerable 
significance. 

Alternation  appears  in  varying  degrees.  The  variation  in  the 
pressure  values  of  the  successive  waves  is  never  very  great  (5-10 
mm.  Hg.).  The  larger  differences  are  easily  detected  by  the  finger; 
the  smaller  can  be  made  out  only  by  the  aid  of  instruments  of 
precision.  It  may  be  continuous  for  hours  or  days,  or  may  be  de- 
tected only  in  short  runs  of  a  few  beats.  It  is  associated  with 
many  other  cardiac  irregularities.  It  often  appears  in  a  few  beats 
following  an  extrasystole  and  then  is  lost  until  introduced  by  an- 
other extrasystole.  It  has  a  tendency  to  become  more  evident  when 
the  heart  rate  is  quickened  and  to  disappear  as  the  heart  becomes 
slower.     One  often  sees  alternation  of  the  pulse  in  patients  suffer- 


A  1. 1  ERNATION 


"J5 


Radial 


Figure  148 

Alternation  of  radial.  The  electrocardiogram  suggests  that  there  is  a  le=ion  of  one 
branch  of  the  A-V  bundle.  Complex  (x)  appears  to  be  of  a  more  normal  form,  but  this 
type  of  beat  was  very  unusual   in  this  patient. 


•"+..'.             ±    ...... .       + 

* 

*         *:-:  _'     a          Jt_ 

| 

' 

0.  A  .f£c<}n^ 

;  ,1 

Radial 


Figure  149 
Radial  shows  alternation.     No  evidence  of  alternation  in  the  electrocardiogram. 


io,6  Alternation 

ing  from  advanced  nephritis  when  they  are  first  admitted  to  the 
hospital,  which  disappears  after  twenty-four  hours'  rest  in  bed. 

PROGNOSIS 

Most  observers  arc  in  agreement  that  alternation  is  a  sign  of 
very  grave  import.  This  certainly  holds  for  the  well-marked  alter- 
nation, which  is  usually  detected  by  palpation  and  which  con- 
tinues for  long  periods.  While  in  some  cases  this  may  be  prac- 
tically the  only  sign  of  the  failure  of  the  heart  to  carry  its  load, 
other  signs  are  usually  present,  such  as  angina,  dyspnoea,  periodic 
breathing,  oedema,  etc.  All  these  emphasize  the  seriousness  of  the 
changes  in  the  myocardium.  But  even  without  these  concomitant 
symptoms,  a  well-marked  continuous  alternans  should  arrest  the 
examiner's  attention  and  lead  him  to  offer  an  extremely  guarded 
prognosis. 

The  lesser  grades  of  alternation,  those  which  are  not  persistent, 
those  which  are  made  evident  only  when  the  heart  rate  is  very 
greatly  accelerated,  and  those  which  occur  during  the  acute  infec- 
tions, but  which  are  not  prolonged  for  any  considerable  time,  prob- 
ably  should  be  regarded  as  much  less  significant  of  grave  myocardial 
defect.  As  yet  these  cases  have  not  been  studied  in  sufficient  num- 
bers or  followed  up  carefully  enough  to  permit  us  to  draw  more 
definite  conclusions  in  regard  to  the  prognosis. 

As  I  have  already  suggested,  further  study  may  show  us  that 
in  one  case  alternation  is  due  to  or  associated  with  a  defective 
conduction,  while  in  another  abnormal  irritability  may  be  the  prom- 
inent associated  change.  It  may  be  that  on  the  basis  of  such  a 
classification  this  sign  may  have  a  new  value  in  prognosis. 

In  a  study  of  the  largest  number  of  cases  by  a  single  observer, 
White*  found  alternation  in  33  per  cent,  of  all  the  heart  cases 
showing  any  degree  of  cardiac  decompensation,  in  which  he  se- 
cured graphic  records.  When  his  report  was  made,  sufficient  time 
had  not  elapsed  to  permit  him  to  draw  accurate  conclusions  as  to 
the  ultimate  outcome  of  his  cases. 

Lewis  regards  alternans  as  an  evidence  of  a  disproportion  be- 
tween the  ability  of  the  heart  muscle  and  the  work  it  is  called 
upon  to  perform.     Hence,  this  irregularity  may  become  manifest 

*Am.  Jour.   Med.   Sc,   1915,  cl,  82. 


Alternation 


i'J7 


Figure  150 

Tachycardia  rate  156.  The  electrocardiogram  shows  alternation  in  the  amplitude  of 
the  R  deflections.  Note  that  the  short  R  is  a  trifle  nearer  the  succeeding  than  the 
preceding  tall  R. 


Figure  151 

From   a  case   of   paroxysmal   ventricular   tachycardia,      Rate    ^05.      The   electrocardio- 
gram shows  alternation. 


io8  Alternation 

when  the  heart  muscle  is  reasonably  healthy,  if  the  demands  upon 
it  arc  excessive,  and  also  when  the  diseased  or  poisoned  muscle  is 
endeavoring  u>  perform  work  of  which  it  is  hardy  capable.  In 
cases  of  paroxysmal  tachycardia,  in  which  on  the  strength  of  other 
evidence  we  feel  reasonably  sure  that  the  ventricular  muscle  is  not 
seriously  damaged,  an  alternation  of  the  heart  is  of  much  less  sig- 
nificance than  when  it  appears   in  a  heart  with  a  slow  rate. 

[f  we  consider  only  these  hearts  with  a  slow  rate,  our  personal 
experience  would  agree  with  that  of  Yaquez,*  who  finds  three 
degrees  of  alternation  which  may  he  arranged  in  the  order  of  their 
prognostic  value,  as  follows:  (i)  Prolonged  continuous  alterna- 
tion; (2)  post-extrasystolic  alternation;  (3)  transitory  alternation. 
A  fatal  termination  may  he  expected  in  continuous  alternation 
within  a  few  months.  I  know  of  no  case  of  this  kind  in  which  death 
has  been  delayed  more  than  two  years. 

*XVTI,  Intcrnat.  Congress  of  Medicine,  London,  1913,  vi,  164. 


CHAPTER  XIV 

The  Influence  Exerted  by  the  Extracardial  Nerves 

In  discussing  the  theories  of  the  nature  of  the  heart  beat,  it  was 
pointed  out  that  the  cells  of  the  myocardium  intrinsically  possess 
the  fundamental  properties  through  which  the  activities  of  the  heart 
are  initiated  and  maintained ;  these  are  modified  and  adapted  to 
the  momentary  needs  of  the  body  through  the  agency  of  the  extra- 
cardial nerves.  It  is  conceivable  that  a  departure  from  the  normal 
efficiency  of  this  adjustment  may  arise  in  two  quite  distinct  ways: 
(i)  The  muscle  cells  may  be  so  changed  that  one  or  more  of  their 
fundamental  properties  may  be  more  than  normally  sensitive  to 
nerve  influences;  (2)  the  nerve  mechanism  may  be  defective,  and 
modifying  influences  abnormally  large  or  small  may  thus  be  brought 
to  bear  on  the  cells  of  the  myocardium. 

It  is,  therefore,  important  that  we  should  examine  the  manner 
in  which  the  myocardial  activities  are  modified  by  the  extracardial 
nerves  and  the  clinical  manifestations  which  are  the  result. 

ANATOMY  AND   PHYSIOLOGY 

The  extracardial  nerves  which  modify  the  activity  of  the  heart 
are  the  cardiac  branches  of  the  two  vagi  and  branches  of  the  cervi- 
cal sympathetics.  The  vagus  arises  from  nuclei  lying  in  the  medulla 
in  the  lower  part  of  the  floor  of  the  fourth  ventricle,  passes  out 
of  the  medulla  in  a  groove  between  the  restiform  and  olivary  body, 
escapes  from  the  skull  through  the  jugular  foramen  and  passes 
down  the  neck  in  the  sheath  of  the  carotid  artery.  About  the  level 
of  the  lower  border  of  the  thyroid  cartilage  the  nerve  is  joined 
by  branches  of  the  sympathetic;  at  the  level  of  the  first  rib  the 
cardiac  branches  are  given  off;  on  the  right  side  they  follow  the 
sheath  of  the  innominate  artery  and  on  the  left  pass  in  front  of 
the  aorta,  thus  reaching  the  cardiac  plexus. 

The  sympathetic  fibers  come  from  the  spinal  cord  bv  way  of 
the  four  or  five  upper  thoracic  spinal  roots  and  pass  through  the 
first  thoracic  ganglion  either  to  the  inferior  cervical  ganglion  or 

199 


200      Influences  Exerted  ijv  the  Extracardial  Nerves 

directly  to  join  the  main  vagus  trunk.     The  fibers  derived  from 

the  sympathetic  arc  known  as  the  accelerator  nerves  of  the  heart. 

The  cardiac  plexus  is  composed  of  nerve  fibers  which  can  be 

traced  over  the  posterior  surface  of  the  auricles  and  over  the 
auricnlo-ventricnlar  groove  to  the  ventricles.  The  ultimate  dis- 
tribution of  the  vago-sympathetic  fibers  is  not  entirely  clear,  bul 

the  recent  work  of  Keith  and  Flack,  <  )|>]>enheim,  Dogicl  and  Colin 
strongly  suggest  that  some  of  them  terminate  in  the  muscle  cells 
of  the  sino-auricular  node,  while  others  end  in  the  node  of  Tawara 
or  follow  the  bundle  of  His  and  its  branches  into  the  muscle  cells 
of  the  ventricles.  These  histological  studies  suggest  that  the  spe- 
cialized muscle  cells  of  the  nodes  and  .-]-/'  bundle  play  an  impor- 
tant role  in  receiving  the  modifying  impulses  conveyed  to  the  heart 

by  the  vago-sympathetic  nerves. 

Stimulation  of  the  vagi  causes  (i)  a  slowing  of  auricles  and 
ventricles,  (2)  a  depression  of  conductivity,  and  (3)  probably  a 
diminution  in  force  of  the  contractions  of  the  left  ventricle.  Stim- 
ulation of  the  sympathetica  causes  an  acceleration  of  the  heart  rate. 

Studies  on  the  activities  of  the  extracardial  nerves  have  revealed 
marked  functional  differences  in  the  right  and  left  vagus  and  in 
the  two  sympathetica.  These  differences  are  qualitative,  as  well  as 
quantitative.  Thus,  in  his  experimental  work  on  dogs,  Cohn*  found 
that  stimulation  of  the  right  vagus  usually  caused  the  arrest  of  all 
the  chambers  of  the  heart,  but  appeared  to  have  very  slight  direct 
influence  either  on  conduction  or  the  activities  of  the  ventricle.  On 
the  other  hand,  stimulation  of  the  left  vagus  had  only  a  moderate 
slowing  effect  on  the  auricles,  but  a  very  definite  depressing  influ- 
ence on  the  rate  of  conduction  between  auricles  and  ventricles.  His 
conclusions  as  to  the  differences  in  the  distribution  of  the  fibers 
of  the  right  and  left  vagi  are  shown  in  Figure  152. 

Rothberger  and  Winterbergf  have  shown  that  a  corresponding 
difference  exists  in  the  distribution  of  the  right  and  left  sympathetic 
fibers,  stimulation  of  the  right  stellate  ganglion  caused  an  increased 
auricular  rate  without  conduction  changes,  while  stimulation  of  the 
left  stellate  ganglion  shortened  or  abolished  the  conduction  time, 
calling   forth  the  suggestion  that  the  irritability  of  the  A-V  node 

*Jour.   Exp.   Med.,    1912,   xvi,   72>2- 

tArch.  f.  d.  ges.  Physiol.,  1911,  cxli,  217;  1910,  exxxv,  506,  559. 


Influences  Exerted  by  the  Extracardial  Nerves     201 


■RIGHT 

SrMTATHCTC 

I'M 

•I!:! 


LEFT 
4rriPA7HETlC 

I'iii 


Figure  152 

Diagram  after  Cohn  (modified)  indicating  the  distribution  of  the  fibers  of  the  right 
and  left  vagi  and  the  right  and  left  sympathetics.. 

It  is  to  be  noted  that  the  right  vagus  and  the  right  sympathetic  are  in  the  main 
distributed  to  the  sino-auricular  node  and  the  auricle.  The  left  vagus  and  the  left  sym- 
pathetic have  a  preponderating  influence  over  the  auriculo-ventricular  node  and  bundle. 
The  data  upon  which  this  diagram  is  based  were  obtained  principally  from  the  conclu- 
sions drawn   from   their  experimental   work  by    Cohn   and  by    Rothberger   and   Winterberg. 


202        [NFLUENCES   EXERTED   BY   Tin:   EXTRACARDIAL   NERVES 

had  been  thus  increased  so  that  it  had  assumed  the  role  of  pace- 
maker for  the  heart.  The  inferences  as  to  the  distribution  of  the 
fibers  cit"  the  sympathetic,  drawn  from  the  observations  of  Koth- 
berger  and  Winterberg,  have  been  incorporated  in  the  diagram 
|  Figure  [52). 

Antedating  the  experimental  work  above  outlined,  Robinson  and 
Draper  J  had  shown  that  in  man  right  and  left  vagus  pressure  pro- 
duced distinct  qualitative  differences.  Their  method  was  to  make 
digital  pressure  over  the  carotid  sheath  sufficient  to  obliterate  the 
carotid  pulse.  They  concluded  from  their  electrocardiographic 
studies  that  the  right  vagus  had  a  more  evident  influence  on  the 
rate  and  force  of  ventricular  contractions,  and  that  the  left  vagus 
had  a  pronounced  effect  in  modifying  conduction.  Clinically,  vagus 
pressure  should  be  employed  only  on  one  side  at  a  time;  alarming 
standstill  of  the  heart   may   result    from  bilateral  pressure. 

The  contrast  in  the  effect  of  the  activities  of  the  right  and  left 
vagi  are  shown  in  Figures  153  and  154.  Both  of  these  records 
were  obtained  from  a  case  of  paroxysmal  tachycardia.  The  arrows 
indicate  the  time  at  which  vagus  pressure  was  made.  Figure  153 
was  taken  during  pressure  on  the  right  vagus;  Figure  154,  during 
pressure  on  the  left  vagus.  The  tachycardia  was  caused  by  a 
very  rapid  auricular  activity  to  which  the  ventricle  made  a  corre- 
sponding rapid  response.  Pressure  on  the  right  vagus  (Figure  153) 
immediately  changed  the  rate  of  the  pacemaker  from  172  to  56  per 
minute.  In  Figure  154  is  shown  the  effect  of  left  vagus  pressure: 
the  ventricular  rate  is  immediately  changed  from  172  to  86,  but 
it  is  evident  that  the  mechanism  of  the  altered  function  is  quite 
different  from  that  shown  in  Figure  153.  The  auricular  rate  is 
unchanged,  hut  the  ventricle  responds  only  to  every  other  auricular 
impulse.  Alternate  auricular  impulses  are  blocked,  hence  the  ven- 
tricular rate  is  halved.  Flere  it  is  evident  that  stimulation  of  the 
right  vagus  exerted  its  influence  mainly  on  the  auricle,  stimulation 
of  the  left  vagus  had  no  effect  on  the  auricle,  but  modified  the  A-V 
junctional  tissues  in  such  a  way  that  a  partial  block  was  induced. 
Numerous  attacks  of  tachycardia,  while  this  patient  was  under  ob- 
servation, permitted  us  to  repeat  these  observations  on  a  number 
of  occasions. 

tjour.  Exp.  Med.,  191 1,  xiv,  217;  1912,  xv,  14. 


!  h. 


1 


Ihf*  saLLk 

I:  iilKl 
will      ;, 


2^ 

«   Eg 


pti 


££ 


c3  s 


«5 


203 


.j     C    u 


J04      Influences  Exerted  by  the  Extracardial  Nerves 

Ashner*  first  observed  that  pressure  on  the  eyeball  caused  a 
slowing  of  the  pulse.  He  traced  the  course  of  these  nerve  im- 
pulses through  the  trigeminus  to  its  nucleus  and  thence  by  fibers 
to  the  vagi.  This  oculocardiac  reflex  has  been  studied  by  many 
observers;  a  digest  of  their  work  may  he  found  in  Levin's  paper. f 
In  general,  when  the  nerve  tracts  are  intact,  right  and  left  ocular 
pressures  correspond  rather  closely  in  their  effects  to  right  and 
left  vagus  pressures   (Figures   155  and   150). 

CLINICAL  TYPES 

The  "accelerated  heart"  and  its  relation  to  vagus  and  sympathetic 
activities  have  been  discussed  in  a  preceding  chapter  and  need  not 
detain  us  at  the  present. 

The  slow  regular  heart,  with  a  rate  of  60  or  somewhat  less,  is 
a  type  often  seen.  It  has  been  referred  to  in  an  earlier  chapter 
(VI)  and  is  usually  due  to  excessive  vagus  influence  constantly  at 
work.  It  has  little  significance,  except  as  an  indication  of  a  high 
degree  of  vagus  tone. 

The  slow  heart,  with  or  without  sinus  arrhythmia,  significant  of 
heightened  vagus  activity,  is  not  infrequently  met  with  in  associa- 
tion with  other  symptoms  suggestive  of  excessive  vagus  influence. 
These  symptoms  are:  paleness  of  the  face,  tendency  to  myopia,  low 
blood  pressure,  moist  skin,  asthma,  gastric  hypersecretion,  hyper- 
chlorhvdria,  rapid  gastric  motility,  spasmodic  constipation,  etc. 
Patients  presenting  this  symptom  complex  have  been  grouped  under 
the  term  "hvpervagotonic."  Over  against  the  group  comprised  in 
this  syndrome  one  sees  many  patients  presenting  an  opposing  series 
of  symptoms  :  tachycardia,  flushing  of  the  skin,  gastric  hyposecre- 
tion,  etc.  It  is  believed  that  these  patients  are  the  subjects  of 
increased  sympathetic  activity,  hence  they  have  been  classified  as 
"hvpersympathicotonics."  These  groups  may  further  he  distin- 
guished by  their  reaction  to  drugs.  The  "hypcrvagotonic"  group 
react:  to  the  administration  of  atropine  by  increased  pulse  rate, 
relief  of  asthmatic  breathing,  diminished  gastric  secretion,  motility, 
etc.,  to  pilocarpin  with  sweating,  salivation,  etc.  The  symptoms  of 
the  "hypersympathicotonics"  are  aggravated  by  the  administration 

*Wien.  klin.  Wochnschr.,  1908,  xliv,  1529. 
fArch.  Int.  Med.,  1915,  xv,  738. 


ttril 


205 


M\ 


¥  t 

: 


fe 


2o6      Influences  Exerted  by  tiie  Extracabdial  Nerves 

of  atropine :  they  do  not  react  to  pilocarpin,  but  respond  to  epine- 

phrin  with  tachycardia,  hypertension  and  glycosuria.  As  a  rule, 
the  "hypervagotonics"  show  a  marked  response  to  vagus  ami  ocular 
pressure;  in  the  "hypersympathicotonics"  these  reflexes  are  dimin- 
ished or  absent.  Such  studies  assist  us  in  formulating  our  impres- 
>ions  as  to  the  relative  importance  of  the  extracardial  reflexes  in 
modifying  the  cardiac  activity  in  the  individual  case.  With  such 
abnormal  tone  either  of  the  vagus  or  of  the  sympathetic  mechanism, 
one  may  feel  less  suspicion  that  an  altered  myocardium  is  respon- 
sible  for  the  changed   heart  activity. 

Figures  155  and  156  are  parts  of  a  continuous  curve  and  afford 
a  record  of  the  effect  of  right  ocular  pressure  secured  in  a  young 
man  of  22  of  the  hypervagotonic  type.  His  usual  heart  rate  was 
under  60,  with  a  moderate  degree  of  sinus  arrhythmia.  He  was 
the  subject  of  attacks  of  asthma,  gastric  hypersecretion  and  hyper- 
acidity and  constipation.  At  the  point  in  the  electrocardiogram 
marked  by  the  arrow,  (1)  pressure  was  made  on  the  right  eye- 
ball, which  was  released  at  (2).  After  the  beginning  of  the  pres- 
sure there  was  one  normal  heart  beat;  from  this  point  until  the 
pressure  was  released,  the  auricle  was  in  complete  arrest,  as  indi- 
cated by  the  absence  of  the  P  wave.  After  a  complete  cardiac 
standstill  of  3.4  seconds,  there  is  a  "ventricular  escape,"  (a)  fol- 
lowed by  two  similar  phenomena  (b)  and  (c)  with  intervening 
periods  of  standstill  each  somewhat  over  two  seconds. 

The  "ventricular  escape"  is  of  such  a  form  that  we  feel  assured 
that  it  originated  from  a  point  high  up  in  the  A-V  bundle,  prob- 
ably in  the  region  of  the  A-V  node.  It  is  another  illustration  of 
the  ability  of  the  cells  of  the  myocardium  other  than  the  sinus  node 
to  initiate  contractions. 

On  the  removal  of  the  ocular  pressure,  the  sinus  node  resumes 
its  pacemaking  function  and  auricular  contractions   (P)   reappear. 

The  most  common  irregularity  of  the  heart  which  is  due  to  vagus 
influences  is  the  "respiratory  sinus  arrhythmia"  of  children  and 
of  young  adults  (Figures  157,  158,  159  and  160).  This  is  fre- 
quently discovered  when  palpating  the  radial.  It  consists  in  a 
rhythmic  lengthening  and  shortening  of  the  heart  cycles  coincident 
with  the  respiratory  movements  of  the  chest;  the  longest  cycles 
usually  appear  in  expiration ;  during  inspiration  the  cycles  are  per- 


Influences  Exerted  by  the  Extracardial  Nerves      207 


ration 


Brachial 


0.2   second 


Figure  157 

Respiratory    sinus   arrhythmia.      Upper    curve    respiratory    movements.      Lower    curve 
brachial  pulse.     Time  0.2  second. 


Jugular 


Figure  158 

Respiratory  sinus  arrhythmia.  Upper  curve  jugular  pulse.  Lower  curve  brachial 
pulse.  Time  0.2  second.  Rhythmic  variation  in  length  of  cycles  vanes  with  respiration. 
The  auricle  participates  in  the  irregularity,  the  a-c  interval  is  normal. 


jo8      Influences  Exerted  by  the  Extracardial  Nerves 

ceptibly  shortened.  Forced  respiration  may  produce  an  arrhythmia 
hitherto  unnoticed  or  may  exaggerate  an  irregularity  which  has  horn 
present  during  natural  breathing.  The  most  pronounced  modifica- 
tion can  be  secured  by  having  the  patient  take  a  full  inspiration 
and  hold  the  breath  for  15  to  30  seconds;  while  holding  the  in- 
spired air  the  pulse  becomes  slow  and  suddenly  quickens  when 
respiration   is   resinned. 

Figure  i<>i  i>  the  electrocardiogram  of  a  boy  of  i->  who  ordi- 
narily showed  a  mild  degree  of  sinus  arrhythmia.  To  verify  the 
nature  of  the  irregularity,  under  instructions  he  drew  a  deep  in- 
spiration at  (I)  and  held  his  breath;  at  (3)  expiration  was  al- 
lowed. The  slowing  of  the  auricles  and  of  the  whole  heart  is 
quite  evident.  There  was  a  distinct  change  in  the  form  of  the  P 
wave  while  the  breath  was  held  (2)  and  this  did  not  recover  its 
normal  contour  until  natural  breathing  was  resumed  (4). 

This  is  the  only  common  forme  of  cardiac  irregularity  met  with 
in  young  children  and,  hence,  has  been  named  by  Mackenzie  the 
"youthful  arrhythmia."  It  is  also  not  infrequently  seen  in  young 
adults,  particularly  in  those  with  a  rather  unstable  nervous  organ- 
ism. The  irregularity  is  due  to  changes,  induced  by  varying  de- 
grees of  intrathoracic  pressure,  in  the  vagus  influences  conveyed 
to  the  sinus  node,  thus  modifying  the  rate  of  impulse  formation 
of  the  pacemaker  of  the  heart. 

This  irregularity  is  sometimes  in  evidence  in  patients  showing 
abnormal  types  of  respiration.  Figure  162  was  obtained  from  a 
man  of  50  with  an  advanced  grade  of  nephritis  exhibiting  Cheyne- 
Stokes  respiration.  The  change  in  pulse  rate  during  the  transi- 
tion from  deep  breathing  to  a  period  of  apnoea  is  illustrated  in 
the  tracing.  During  the  active  respiratory  movements,  the  heart 
cycles  occupied  1.4  seconds;  during  apncea,  the  rate  increased 
so  that  each  cycle  consumed  approximately  0.6  second.  It  is  prob- 
able that  in  this  case  the  change  in  vagus  tone  is  central  in  origin, 
depending  on  the  accumulation  of  carbon  dioxide  in  the  blood; 
the  heart  has  endeavored  thus  to  compensate  for  the  disordered 
respiratory  function. 

The  graphic  records  of  a  case  in  which  the  arrhythmia  was 
due  to  peripheral  stimulation  of  the  vagus,  are  presented  in  Figure 
163.     This  was  secured  from  an  extremely  neurotic  young  man  of 


% 


1 


\m 


m  - 


£'    E 


fe         " 


209 


ff   - 


(H    — 


, 


•  5 


^1 


jio      Influences  Exerted  by  the  Extracardial  Nerves 

22,  who  was  seen  in  consultation  because  it  was  thought  that  he 
was  suffering  from  auricular  fibrillation  on  account  of  the  com- 
plete irregularity  of  the  pulse.  The  upper  curve  of  the  record 
was  obtained  by  placing  a  receiving  cup  over  the  upper  part  of 
the  neck.  The  movements  are  due  to  the  efforts  of  the  patient  to 
swallow  and  expel  air  from  the  stomach.  The  change  in  the  cardiac 
cycles  are  clearly  synchronous  with  these  irregular  movements  of 
the  (esophagus.  Electrocardiograms  showed  conclusively  that  the 
complete  irregularity  of  the  heart  was  not  due  to  auricular  fibril- 
lation,  but  was  caused  by  the  varying  rate  of  stimulus  production 
in  the  normal  pacemaker,  induced  by  the  spasmodic  muscular  move- 
ments  during  "cribbing." 

The  identification  of  this  form  of  irregular  pulse  is  usually  a 
simple  matter.  The  rhythmic  change  in  the  length  of  the  cycles 
is  synchronous  with  respiration,  and  may  be  exaggerated  by  forced 
respiratory  movements.  The  pulse  waves  usually  show  very  slight 
variations  in  size ;  the  only  noticeable  departure  from  the  normal 
is  the  rhythmic  variation  of  the  intervals  between  the  beats.  The 
cardiac  irregularity  is  of  the  same  nature,  first  and  second  sounds 
follow  each  other  at  normal  equal  intervals,  but  the  time  interval 
between  the  second  and  first  sounds  shows  a  rhythmic  change  in 
length.  The  venous  pulse  (Figure  158)  shows  a  normal  succes- 
sion of  a,  c  and  v  waves,  but  the  intervals  between  these  groups 
show  the  same  grade  of  irregularity  as  the  arterial  pulse.  The 
electrocardiogram  (Figures  159,  160  and  161)  presents  a  series  of 
normal  auricular  and  ventricular  complexes.  The  ventricular  curves 
are  of  normal  duration,  and  the  irregularity  shows  a  departure  from 
the  usual  physiological  rhythm  only  in  a  variation  in  the  length 
of  the  diastolic  period. 

From  the  evidence  presented  in  regard  to  the  relative  influences 
of  the  right  and  left  vagus  nerves  on  the  sinus  node  and  on  the 
junctional  tissues,  it  may  be  inferred  that  the  right  vagus  is  the 
most  important  factor  in  producing  this  irregularity.  Exceptionally 
one  meets  with  a  case  of  "sinus  arrhythmia"  in  which  the  poly- 
gram shows  an  a-c  interval  of  varying  length,  the  electrocardio- 
gram a  similarly  changing  P-R  interval.  This  indicates  that  the 
passage  of  stimuli  from  the  auricle  to  the  ventricle  has  been  de- 
layed and  in  these  one  is  led  to  the  conclusion  that  the  tone  of 


21  I 


~  a 

ni  o 


— — 
5-s 


S«H 


1 

J 

5   i 

E  rt 

K  3 

IJl:- 

"i 

Q^:^:$ 

u 

a 

212      Influences  Exerted  by  the  Extra<  vrdial  Nerves 

the  loft  vagus  also  is  being  rhythmically  modified,  thus  affecting 
the  rate  of  the  ventricular  response. 

rhe  clinical  significance  of  "respiratory  sinus  irregularities"  is 
mtv  slight.  The  importanl  element  is  the  recognition  of  their 
true  character,  thus  distinguishing  them  from  the  forms  of  abnor- 
mal cardiac  activity  of  a  more  serious  nature. 

Patients  showing  this  arrhythmia  do  not  develop  cardiac  insuffi- 
ciency which  can  be  attributed  to  the  irregularity.  Ii  is  frequently 
met  with  in  neurasthenics  in  whom  no  other  evidence  of  cardiac 
abnormality  can  be  found  at  the  time,  or  subsequently.  In  the 
majority  of  children  it  will  spontaneously  disappear  before  puberty. 
It  has  been  studied  in  robust  school  hoys,  soldiers  in  training  and 
other  healthy  individuals.  It  is  not  indicative  of  myocardial  dis- 
ease and  requires  no  treatment.  No  drugs  or  other  therapeutic 
measures  are  needed,  nor  should  those  who  present  this  symptom 
limit  their  customary  activities. 

Then-  is  another  considerable  group  of  sinus  arrhythmias  which 
hear  no  relation  to  the  respiratory  movements.  These  disorders 
of  the  heart  mechanism  have  been  classified  in  subgroups  by  Lewis 
as  follows:  (i)  sudden  cessation  of  the  whole  heart  heat;  (2) 
phasic  variations  of  pulse  rate,  in  which  a  retardation  and  subse- 
quent gradual  acceleration  of  the  whole  heart  occurs;  (3)  an  ir- 
regularity of  the  whole  heart  in  which  shorter  and  longer  pauses 
are  mingled  indiscriminately. 

(1)  Sudden  cessation  of  the  whole  heart  heat.  This  is  a  form 
of  irregularity  which  is  seen  with  extreme  rarity.  It  has  been 
known  as  "sino-auricular  block,"  since,  on  rather  theoretical 
grounds,  it  was  supposed  to  be  duo  to  an  interference  with  the 
passage  of  the  impulse  from  the  sinus  node  to  the  auricular  tissues. 
The  phenomenon  consists  in  the  dropping  out  of  a  single  heat; 
that  is  to  say,  there  is  a  pause  during  which  there  is  no  evidence 
of  activity  of  any  part  of  the  heart.  The  length  of  this  pause 
is  commonly  a  trifle  less  than  two  heats  of  the  usual  rhythm. 
Since  at  present  we  have  no  means  of  detecting  the  activity  of 
the  sinus  node  other  than  the  effects  which  it  has  on  the  auricle, 
there  seems  to  be  no  direct  way  of  establishing  the  fact  that  the 
node  continues  its  normal  activity  hut  that  its  stimulus  is  inter- 
rupted on  the  way  to  the  auricle.     From  the  close  similarity  which 


2/3 


1 

p 

6 

£ 

1 

H 

1 

6 

u 

1 

d. 

1 

E 

nj 

PI 

* 

g 

3 

u 

»3 

a 

I 

o 

S 
(>. 

Ih 

o 

Figure  162 

pper    curve     respir 
ut  43  per  minute. 

PS 

§8 

•-  c 

«  & 

.is  £ 

D.T3 

4;  u_t 

1-  0 

^  to 

c  rt 
>> 

u° 

■58 
0. 

in  rt 
.tS   tj) 

Js.s 

0  3 
CO 

(*-  +■* 
0  n) 

°o 

C3 

0 

0 
■ 

-M4      Influences  Exerted  by  the  Extracardial  Nerves 

this  phenomenon  seems  to  bear  to  the  irregularities  (phasic  folia- 
tions oj  pulse  rate)  discussed  in  the  next  paragraph,  since  these 
two  types  of  irregularity  are  seen  in  the  same  patient,  since  in 
certain  cases  (Eyster  and  Evans)*  it  can  be  induced  by  pressure 
on  the  right  vagus  nerve  and  abolished  by  atropine,  it  seems  to 
me  there  is  little  doubt  that  it  is  a  vagus  effect  and  the  term  "sino- 
auricular  block"  should  be  dropped  as  inconsistent  with  the  evi- 
dence which  we  possess  at  the  present  time. 

This  irregularity  can  be  surely  recognized  only  by  instruments 
of  precision.  The  polygraph  shows  an  absence  of  ventricular  activ- 
ity in  both  arterial  and  venous  tracings.  The  jugular  record  shows 
no  evidence  of  an  a  wave  during  the  pause. 

The  electrocardiogram  merelv  shows  a  pause  nearly  or  quite 
equal  to  two  cycles  of  the  usual  cardiac  rhythm  without  evidence 
of  either  auricular  or  ventricular  activity. 

This  irregularity  is  usually  associated  with  other  evidences  of 
abnormal  cardiac  function,  most  of  the  reported  cases  have  shown 
some  degree  of  auriculo-ventricular  block. 

Figure  [65  is  the  record  (lead  1  )  of  a  man  of  55  with  evidences 
of  myocardial  degeneration.  At  other  times  he  had  showed  ex- 
treme grades  of  cardiac  arrhythmia  with  many  ventricular  cxtrasys- 
toles,  paroxysmal  tachycardia,  etc.,  etc.  At  the  time  the  record 
was  taken  he  had  recovered  to  a  considerable  degree  and  the  heart 
was  for  him  fairly  regular  and  for  weeks  showed  only  the  abnor- 
malities here  presented.  It  is  to  he  noted  that  the  P  wave  is 
slightly  diphasic,  that  the  R  wave  is  reversed,  that  the  whole  ven- 
tricular complex  has  a  very  abnormal  form  and  the  P-R  interval 
is  excessively  long.  One  "dropped  beat"  is  evident  in  the  electro- 
cardiogram. The  interval  including  the  "dropped  heat"  (  R.,  to  Rt) 
is  a  trifle  less  than  the  length  of  two  cycles  of  his  usual  rhythm 
(R,  to  R,). 

The  record  (Figure  164)  of  a  young  girl  suffering  from  rheumatic 
pericarditis  shows  a  prolonged  standstill  of  the  heart.  At  other 
times  the  change  in  the  length  of  the  cardiac  cycles  was  less  abrupt, 
so  that  one  would  have  included  her  arrhythmia  under  group  2, 
"phasic  variations  of  the  pulse  rate";  indicating,  as  we  have  already 
suggested,  that  no  sharp  line  may  fairly  be  drawn  between  these 

•Arch.   Int.   Med.,   1915,   xvi,  832. 


FlGUKE    164 
Sinus    arrhythmia    nnt    respiratory.      "Dropped    beat, 
rheumatic  pericarditis.     P-R  interval  =  o.2  second. 


From    a    younf?    woman    with 


Figure  165 

(<       From   a  man   55   years  old  with  myocardial  degeneration.      "Dropped   beat."      So-called 
sino-auncular    block."      All    the    complexes    are    very    atypical    (see    text).      P-R   intervals 
0.22  second.      Time  0.2   second. 


Figure  166 

Records  from  above  downward  jugular  tracing,  electrocardiogram,  brachial  tracing, 
time  0.2  second.  From  a  young  woman  with  hyperthyroidism.  The  arterial  pulse  is 
completely  irregular,  but  both  the  jugular  and  electrocardiographic  records  indicate  an 
auricle   with    irregular   but   otherwise    normal   contractions. 


jio      Influences  Exerted  by  the  Extracardial  Nerves 

groups.  The  somewhat  prolonged  P  R  interval  suggests  a  hyper- 
tonus  of  the  left  as  well  as  of  the  right  vagus. 

z.  Phasic  variations  of  pulse  rate  (Figures  1^7,  168  and  169). 
1  [ere  there  are  alternating  periods  of  rapid  slowing  and  equally  rapid 
acceleration  of  the  heart.  In  some  cases  this  change  is  quite  rhyth- 
mic, the  heart  beating  10  or  15  times  between  the  individual  cycles 
of  the  maximum  length,  in  other  cases  the  time  elapsing  between 
similar  phases  is  very  variable.  The  variation  in  the  length  of  the 
individual  cycles  is  always  quite  independent  of  respiratory  move- 
ments. 

Wry  little  is  known  of  the  mechanism  of  this  form  of  irregu- 
larity, but  the  evidence  seems  to  point  to  vagus  influences  acting 
on  a  sinus  node  which  is  functionally  damaged.  1  believe  the  mech- 
anism responsible  for  its  production  is  quite  similar  to  that  of  the 
single  dropped  heat  described  above.  The  identification  may  be  sus- 
pected when  a  rhythmic  series  of  quickening  and  slowing  heart  beats 
is  detected  by  palpation  or  auscultation.  The  type  of  irregularity 
is   securely   established   by  graphic   records. 

Figure  [67  is  the  record  of  a  man  with  general  arteriosclerosis, 
with  a  rhythmic  change  which  occupied  about  18  heart  cycles.  Fig- 
ure 168  is  from  a  girl  of  eleven  with  acute  endocarditis;  when  the 
acute  process  subsided  the  arrhythmia  disappeared.  The  electro- 
cardiogram of  a  boy  of  fourteen  with  acute  rheumatic  endocarditis 
and  arthritis  is  reproduced  in  Figure  170.  The  varying  length  of 
the  P-K  interval  in  this  record  is  suggestive  either  of  excessive 
activity  of  the  left  vagus  or  of  an  A-V  node  peculiarly  susceptible 
valescence,  but  reappeared  coincident  with  a  recurrence  of  the 
arthritis. 

5.  Irregularity  of  the  whole  heart  in  which  shorter  and  longer 
pauses  arc  mingled  indiscriminately.  This  arrhythmia  closely  sim- 
ulates the  pulse  features  of  complete  irregularity  of  auricular  fibril- 
lation of  the  slow  type  (Figures  163  and  166).  But  the  mechan- 
ism of  its  production  is  quite  different.  The  sino-auricular  node 
acts  as  the  pacemaker  of  the  heart,  but  the  rhythmic  character 
of  the  formation  of  stimulus-material  is  disturbed,  probably  due 
to  the  reception  of  impulses  varying  in  intensity  which  reach  the 
sinus  node  through  the  right  vagus.     The  auricle  responds  irregu- 


217 


I 

1 


m 


£ 


1 


I 


218      Influences  Exerted  by  the  Extracardial  Nerves 

larly  and  the  ventricle  follows  the  auricular  contractions  with  a  cor- 
responding arrhythmia,  hut  with  no  other  abnormal  features.  In 
short,  the  whole  heart  assumes  the  arrhythmia  of  the  pacemaker, 
hut  the  chambers  respond  sequentially  and  otherwise  normally. 

Recognition  of  this  type  of  irregularity  by  the  ordinary  physical 
signs  is  difficult.  If  the  pulsation  of  the  veins  of  the  neck  are 
prominent,  one  may  he  able  to  detect  the  presystolic  a  wave,  in- 
dicative of  coordinated,  hut  arrhythmic,  auricular  activity.  Barring 
this  resort  must  he  had  to  graphic  records.  Both  polygrams  and 
electrocardiograms  show  nothing  ahnormal  except  the  unequal  dias- 
tolic periods.  The  a,  c  and  v  waves  of  the  jugular  record  show 
the  normal  relationship  (Figure  [66  and  [69).  The  auricular  and 
ventricular  complexes  of  the  electrocardiogram  have  a  normal  se- 
quence and  the  usual  form  (  Figures  K>()  and  171  ).  The  polygram 
is  to  he  distinguished  from  that  of  auricular  fibrillation  by  the  pres- 
ence of  the  auricular  as  opposed  to  the  ventricular  form  of  venous 
pulse;  the  electrocardiogram  shows  a  P  wave  of  normal  type  and 
an  absence  of  the  small  diastolic  oscillations  so  characteristic  of 
auricular  fibrillation.  The  condition  is  to  be  distinguished  from 
the  auricular  cxtrasystole  by  the  absence  of  intervals  which  repre- 
sent pauses  of  a  compensatory  character  and  by  the  normal  contour 
of  the  P  wave  in  the  galvanometric  records. 

The  polygraphs  (Figures  166  and  169)  show  the  complete  ir- 
regularity of  the  arterial  pulse,  an  auricle  which  is  active  and  equally 
arrhythmic,  a  considerable  variation  in  the  length  of  the  diastolic 
period  and  the  normal  sequential  relation  of  auricle  and  ventricle. 

Figure  166  was  from  a  young  woman  of  20  with  symptoms  which 
suggested  hyperthyroidism,  but  with  no  evidence  of  myocardial  dis- 
ease other  than  the  arrhythmia.  The  electrocardiogram  (  Figure 
171)  was  obtained  from  a  woman  of  25  during  an  attack  of  acute 
rheumatic  endocarditis. 

CLINICAL  FEATURES  AND  SIGNIFICANCE 

Sinus  irregularities  which  hear  no  relation  to  respiration  are  seen 
more  frequently  in  the  young,  but  are  not  limited  to  this  period  of 
life.  They  may  be  discovered  accidentally  in  those  who  show  no 
other  evidence  of  disease.  They  are  occasionally  seen  in  the  period 
of  convalescence  following  the  acute  infectious  diseases.     They  are 


Influences  Exerted  by  the  Extracardiai,  Nerves      219 


Jugular 


Brachial 


0.2  second 


Figure  169 

Brachial  and  jugular  tracings  from  a  young  woman  with  a  completely  irregular  pulse. 
Sinus    arrhythmia    independent    of    respiration. 


220      Influences  Exerted  by  the  Extracardial  Nerves 

sometimes  associated  with  the  administration  of  large  doses  of 
digitalis. 

These  irregularities  are  usually  seen  in  association  with  a  slow 
pulse  rate,  sometimes  they  are  abolished  by  exercise  or  a  febrile 

condition  in  which  the  pulse  is  accelerated.  Most  of  them  show 
a  very  prompt  response  to  vagus  or  ocular  pressure  <  Figures  155 
and  156).  Frequently  they  disappear  under  the  administration  of 
atropine. 

At  the  Presbyterian  Hospital,  in  the  routine  examinations  dur- 
ing the  past  \ear,  we  have  studied  and  recorded  graphically  seven- 
teen cases  of  sinus  arrhythmia  in  which  the  irregularities  were  quite 
independent  of  respiratory  movements.  Eight  of  these  cases  were 
associated  with  other  forms  of  arrhythmia  suggesting  a  myocardial 
defect,  such  as  extrasy  stoles,  partial  auriculo-ventricular  block,  etc. 
The  nine  remaining  cases  belonged  exclusively  to  the  type  of  ir- 
regularity now  under  discussion.  Among  these  there  was  one  adult 
and  one  seventeen  ;  the  rest  were  all  under  fourteen  years  of  age. 
Six  were  males  and  three  females.  Of  these  nine  cases,  five  had 
physical  signs  of  definite  endo-  or  pericardial  lesions ;  one  was 
an  overgrown  athletic  boy  with  a  moderate  degree  of  cardiac  hyper- 
trophy, one  had  chorea ;  the  remaining  two  showed  no  definite  signs 
of  disease,  although  one  was  slightly  dyspneeic  and  the-  other  was 
of  a  high-strung,  nervous  temperament.  In  two  of  these  cases  the 
irregularity  disappeared,  in  the  others  it  still  persisted  at  the  time 
of  the  last  examination. 

Clinically,  it  is  important  that  we  should  recognize  the  nature 
of  these  arrhythmias  and  distinguish  them  from  the  types  of  more 
serious  moment  with  which  they  may  he  confounded. 

Such  an  activity  of  the  heart  is  in  itself,  1  believe,  not  a  serious 
matter,  hut  my  present  impression  is  that  it  indicates  a  definite  myo- 
cardial change  which  may  he  very  transitory,  hut  which  may  well 
bear  careful  observation. 

The  exciting  causes  are  undoubtedly  the  nervous  impulses  con- 
veyed  to  the  heart  through  the  vagi,  but  these  are  probably  peculiarly 
effective,  since  they  are  acting  on  a  heart  which  is  damaged  and, 
hence,  unusually  susceptible  to  outside  influences. 


— 


1 


- 


1 


W    £ 


Pi  o 

o 
.•a 

rt  o 

S3« 


1*~1 


tt. 


o 


CHAPTER  XV 

Mixed   Arrhythmias 

In  the  preceding  pages  the  arrhythmias  have  been  discussed  as 
individual  types.  This  is  the  usual  form  in  which  they  are  seen 
in  the  clinic  and  it  is,  perhaps,  simpler  to  study  them  primarily 
from  this  standpoint. 

It  has  been  pointed  out  from  time  to  time  how  close  is  the  asso- 
ciation of  some  of  the  types;  for  example,  that  a  single  heart  may 
pass  through  the  phases  of  extrasystole,  auricular  flutter,  fibrilla- 
tion and  paroxysmal  tachycardia  and  repeat  any  one  of  these  abnor- 
mal types  of  functional  activity. 

There  are  other  instances  by  no  means  rare  in  which  the  arrhyth- 
mia depends  upon  the  alteration  of  more  than  one  of  the  funda- 
mental functions  of  the  cardiac  muscle.  Changes  in  the  rate  of 
stimulus  formation  at  the  sino-auricular  node  are  not  infrequently 
associated  with  a  defect  in  the  capacity  of  conduction  in  the  bundle 
of  His.  Increased  irritability  of  various  portions  of  the  muscula- 
ture, as  evidenced  by  extrasystoles  or  fibrillation,  is  often  found 
associated  with  a  depression  of  the  property  of  conduction.  One 
might  spend  considerable  time  in  enumerating  the  various  combina- 
tions which  are  seen,  but  it  will  suffice  us  to  discuss  several  of  the 
more  common  and  distinctive  types  of  the  mixed  arrhythmias,  bear- 
ing in  mind  that  these  by  no  means  exhaust  the  assortment  that 
are  encountered. 

Perhaps  the  most  common  type  of  the  mixed  irregularities  are 
those  in  which  a  definite  sinus  arrhythmia  is  associated  with  a 
defect  in  the  conductivity  of  the  A-V  bundle.  The  electrocardio- 
gram of  a  well-marked  case  of  this  group  is  shown  in  Figure  172. 
The  lower  line  of  numerals  represent  the  measurements  in  frac- 
tions of  a  second  of  the  P-R  intervals,  the  upper  the  P-P  intervals. 
The  P-R  time  was  usually  excessive  in  this  case  and  in  the  rec- 
ord shows  a  variation  in  length  from  0.18  to  0.43  second.  The  P-P 
intervals,  which  indicate  the  rate  of  stimulus  formation  at  the  sinus, 
also  presents  a  variation  in  length  with  a  tendency  to  a  rhythmic, 
gradual   increase   followed  by  a  diminution  in  the  length  of  these 

222 


9    inSP 


224  Mixed  Arrhythmias 

intervals.  The  extreme  differences  are  about  one-third  of  a  sec- 
ond. The  ventricular  arrhythmia  is  the  roultant  of  these  two  fac- 
tors and  the  cycles  occupy  from  0.69  to  1.01  seconds.  The  arrhyth- 
mia was  accentuated  by  forced  respiratory  movements.  Just  before 
this  curve  was  secured  the  patient  took  a  deep  inspiration  and  held 
the  breath;  the  slow  expiratory  movement  is  indicated  l>v  the  por- 
tion of  the  respiratory  curve  in  the  latter  half  of  the  record.  It  is 
quite  probable  that  the  arrhythmia  is  in  a  large  measure  due  to 
vagus  influences,  the  sinus  activity  varying  with  the  tone  of  the 
right  vagus,  the  conductivity  of  the  bundle  changing  with  the  tone 
of  the  left  vagus  (see  Chapter  XIV  on  the  Influence  of  the  Extra- 
cardial   Nerves). 

In  Figures  173  and  174  are  exhibited  the  electrocardiograms  of 
two  cases  in  which  sinus  arrhythmias  arc  associated  with  changes 
in  the  contour  of  the  P  leaves,  indicating  a  shifting  of  the  pace- 
maker from  the  sinus  node  to  some  other  point  in  the  auricular 
wall.  In  Figure  173  a  small,  but  definite,  change  in  the  P  deflec- 
tion (1,  2,  3,  4)  is  accompanied  by  a  shortening  in  the  P-R  inter- 
val; at  5  the  P  wave  recovers  the  form  characteristic  of  the  normal 
pacemaker  and  the  P-R  interval  measures  0.2  second. 

Figure  174  presents  less  variation  in  the  P-R  interval,  but  a 
more  marked  dislocation  of  the  pacemaker  is  suggested  by  the  com- 
plete inversion  of  the  auricular  complex. 

A  functional  abnormality  of  this  character  indicates  a  mild  de- 
gree of  auricular  myocardial  defect,  not  in  itself  sufficient  to  em- 
barrass the  patient  but  which  serves  as  a  signal  to  the  physician 
that  unless  stationary  it  may  be  the  forerunner  of  more  serious 
damage,  with  corresponding  mischief  to  the  circulation. 

A  mixed  arrhythmia,  which  is  extremely  common,  is  the  asso- 
ciation of  ventricular  extrasystoles  with  auricular  fibrillation.  It 
is  met  with  not  infrequently  in  subjects  with  auricular  fibrillation 
to  whom  digitalis  has  been  administered  in  considerable  doses.  It  is 
also  seen  in  those  who  have  never  received  digitalis.  Most  often 
the  extrasystoles  occur  at  infrequent  intervals  and  are  all  of  one 
type.  The  record  shown  in  Figure  175  was  obtained  from  a  patient 
who  was  not  taking  digitalis.  It  presents  rather  an  extreme  degree 
of  the  irregularity.  The  extrasystoles  are  of  three  distinct  types, 
indicating  as  many  points  of  abnormal  ventricular  irritability.     By 


225 


a  z 

—  — 


226  Mixed  Arrhythmias 

means  ol  the  ordinary  methods  of  physical  examination,  one  may 
find  considerable  difficulty  in  correctly  interpreting  this  type  of  ir- 
regularity. <  me  who  has  studied  a  great  many  hearts  of  this  kind 
learns  to  distinguish  by  auscultation  certain  contractions  which  dif- 
fer from  the  majority  by  their  "flopping"  character,  and  these  he 
may  suspect  to  be  extrasystoles.  They  can  only  be  surely  analyzed 
with  the  aid  of  electrocardiographic  curves. 

The  appearance  of  a  large  number  of  ventricular  extrasystoles 
in  a  case  of  auricular  fibrillation  indicates  that,  in  addition  to  an 
irritable  auricle,  we  have  an  abnormally  irritable  ventricle.  The 
muscle  damage  is  very  extensive.  When  the  extrasystoles  arise 
from  many  foci,  we  must  conclude  that  the  lesions  are  even  more 
widely  distributed.  Nearly  all  of  these  patients  have  a  severe  grade 
of  cardiac  insufficiency  which  is  extremely  difficult  to  control. 

In  discussing  the  prognosis  of  auricular  fibrillation,  it  was  pointed 
out  that  the  future  of  the  patient  depended  to  a  very  large  degree 
on  the  integrity  of  the  ventricular  muscle.  Here  we  have  clear  evi- 
dence that  the  ventricular  wall  is  extensively  diseased.  The  grav- 
ity of  the  prognosis  increases  with  the  multiplication  of  the  num- 
ber and  types  of  ventricular  extrasystoles. 

AURICULAR   FIBRILLATION    AND   HEART  BLOCK 

In  1909  James  Mackenzie*  described  a  group  of  four  cases  pre- 
senting a  slow  rhythmic  pulse  which  suggested  a  complete  heart 
block,  but  in  which  polygraph  curves  failed  to  reveal  any  auricular 
activity.  He  suggested  that  there  was  also  in  these  cases  a  brady- 
cardia of  the  auricle  and  that  the  auricles  and  ventricles  were  con- 
tracting simultaneously  in  response  to  a  stimulus  arising  in  the 
region  of  the  A-V  node.  Accordingly,  he  designated  this  type  as 
"nodal  bradycardia."  This  acute  observation  was  soon  followed  by 
an  exhaustive  study  of  one  of  the  cases  of  this  group  by  Lewis  and 
Mack.t  using  Einthoven's  galvanometer.  They  were  able  to  show 
that  the  auricle  was  in  a  condition  of  fibrillation  and  that  the  ven- 
tricles had  assumed  the  slow  ideo-ventricular  rhythm  ordinarily  seen 
in   complete  heart  block.     The  post-mortem  examination  of   this 

♦Heart,   1909-10,   i,   25. 

tQuart.  Jour.  Med.,  1909-10,  iii,  273. 


M  [xed  Arrhythmias 


227 


Jugular 


Brachial 


Figure  177 

Auricular    fibrillation,    complete    A-V    block    and    ventricular   extrasystoles.      Rate    35. 
For    electrocardiogram    of    this    case    see    Figure    176. 


'    Jugular 


Brachial 


Figure  178 

Auricular    fibrillation    and    complete    A-V    block.       Note    rhythmicity    of    ventricular 
complexes 


228  M  IXED    ARRHYTH  M  IAS 

heart  i  revealed  a  lesion  completely  severing  the  bundle  of  Ilis,  and 
organic  damage  to  the  auricular  wall  sufficient  to  explain  the  ex- 
istence  of  auricular  fibrillation. 

It  has  been  my  fortune  to  observe  two  cases  |  resenting  this 
symptom  complex.  (  >ne  of  these  died  while  under  observation,  but 
permission   for  an  autopsy  could  not  be  obtained. 

The  mechanism  of  this  rather  unusual  functional  activity  seems 
reasonably  clear.  There  are  no  coordinated  contractions  of  the 
auricles;  they  are  in  a  state  of  fibrillation  and,  as  is  usual  in  this 
condition,  irregular  impulses  are  being  constantly  showered  on  tin- 
functional  tissues.  Since,  however,  there  is  a  complete  functional 
severance  of  the  .-/-/'  bundle,  all  these  impulses  are  blocked  and 
none  of  them  reach  the  ventricle.  Thus  cut  off  from  stimuli  de- 
rived from  the  upper  portions  of  the  heart,  the  ventricle  initiates 
its  own  stimuli  and  a  typical  ideo-ventricular  rhythm  becomes 
established. 

Among  the  etiological  factors  found  have  been  syphilis,  rheuma- 
tism and  general  arteriosclerosis.  As  in  other  conditions  of  block, 
the  association  of  mitral  disease  is  more  common  than  other  valvu- 
lar lesions. 

The  effect  of  digitalis  and  drugs  of  the  same  order  in  producing 
a  complete  block  in  cases  of  auricular  fibrillation  will  be  consid- 
ered in  another  place. 

Of  the  cases  reported  in  the  literature  only  one  (  Mackenzie,  case 
4)  was  under  fifty  years  of  age,  the  others  were  from  fifty-one 
to  sixty-eight  years  old.  It  is  seen  less  frequently  in  women  than 
in  men. 

Complete  block  will,  of  course,  be  inferred  when  the  ventricles 
are  found  to  be  beating  rhythmically  at  a  rate  in  the  neighborhood 
of  thirty  per  minute.  When  a  rhythmic  pulsation  of  the  jugulars 
two  or  three  times  the  rate  of  the  ventricles  is  absent,  an  associated 
auricular   fibrillation   may   be   suspected. 

In  the  polygraph  the  arterial  records  show  a  slow  rhythmic  rate 
of  about  thirty  per  minute  and  a  corresponding  rhythmic  jugular 
of  the  ventricular  form.  All  a  waves  are  absent  and  there  is  no 
evidence  of  gross  auricular  activity    (Figure   177). 

The   electrocardiogram    (Figure    [78)    presents  a   slow   rhythmic 

tCohn  and  Lewis:  Heart,  1912-13,  iv,  15. 


Mixki)  Arrhythmias  229 

contraction  of  the  ventricle  characteristic  of  complete  block,  an 
absence  of  all  P  waves  and  the  small  undulations  |  // )  pathog- 
nomonic  of   auricular   fibrillation. 

The  galvanometric  record  of  another  case  is  shown  in  F'gure 
176.  Here  the  activity  is  further  complicated  by  ventricular  con- 
tractions (.x'j,  x2)  originating-  in  abnormal  points  in  the  ventricular 
wall,  indicating  an  excessive  irritability.  The  record  is  suggestive 
of  the  effect,  of  digitalis  when  administered  in  large  doses  to  cases 
of  auricular  fibrillation,  but,  in  this  instance,  neither  digitalis  nor 
any  other  drug  of  this  group  was  being  given.  The  abnormal 
activity  was  entirely  due  to  the  myocardial  defects.  In  this  case 
the  administration  of  atropine  produced  a  considerable  increase  in 
the  ventricular  contractions  of  the  normal  type  (R). 

Further  details  have  been  reported  in  a  paper  on  "Functional 
Heart  Block."*  A  polygram  secured  from  this  same  patient  is  re- 
produced (Figure  177).  The  arterial  pulse  is  slow,  35  per  min- 
ute, and  rhythmic,  except  toward  the  end  of  the  curve,  where  two 
extrasystoles  appear.  The  jugular  tracing  shows  an  absence  of  all 
a  waves  and  is  of  the  ventricular  form. 

Most  of  these  cases  present  signs  of  a  considerable  degree  of 
cardiac  insufficiency,  and  it  is  evident  that  the  defective  myocardium 
is  unable  to  maintain  an  adequate  circulation.  In  neither  of  the 
two  cases  which  I  have  had  under  observation  have  there  been  at- 
tacks of  unconsciousness  or  convudsions,  but  several  of  the  re- 
ported cases  have  exhibited  phenomena  which  allow  them  to  be 
grouped  under  the  Adams-Stokes  syndrome.  The  convulsions  are 
due,  as  in  other  cases  of  heart  block,  to  cerebral  anaemia  follow- 
ing an  abrupt  lowering  of  the  heart  rate. 

In  these  cases  the  myocardial  damage  is  so  extensive  that  it 
makes  the  prognosis  exceedingly  grave.  The  termination  may  occur 
at  any  time  in  a  convulsive  seizure  or,  as  in  the  two  cases  which 
I  have  been  able  to  follow,  the  course  may  be  a  progressively  weak- 
ening heart  with  ultimate  failure. 

Probably  three  or  four  years  would  be  the  longest  period  of  life 
which  could  be  expected  after  the  discovery  of  such  serious  myo- 
cardial defects. 

*Hart:  Amer.  Jour.  Med.  Sc.  1915,  cxlix,  62. 


230  Mixed  Arrhythmias 

HEART  BLOCK    AND   EXTRASYSTOLES 

Aii  unusual  phenomenon  occasionally  met  with  in  cases  of  com 
plete  block  is  presented  in  Figure  [79.  This  was  taken  from  a 
case,  seen  in  consultation  with  Dr.  Frank  Grauer,  of  Adams-Stokes 
disease,  who  died  in  a  convulsion  two  years  after  these  observa- 
tions were  made,  llis  usual  ventricular  contractions  were  per- 
fectly rhythmic  and  at  a  rate  of  thirty  per  minute,  the  auricular 
rate  was  86.  At  rare  intervals  there  appeared  a  single  premature 
ventricular  heat,  sometimes  two  of  these  presented  in  succession. 
That  the  origin  of  these  extra  contractions  must  have  been  in  the 
region  of  the  A-V  node,  or,  at  any  rate,  high  up  in  the  A-V  bundle, 
may  be  inferred  from  the  form  of  the  ventricular  complexes  of 
the  electrocardiogram  (Figure  180),  taken  on  the  same  day.  There 
are  two  possible  explanations  of  this  activity  :  (  1  )  The  block,  which 
is  ordinarily  complete,  occasionally  becomes  partial  and  the  ven- 
tricle responds  with  a  delay  in  the  conduction  period  to  an  auricular 
impulse;  the  complete  character  of  the  block  for  most  of  the  time 
makes  this  explanation  seem  improbable.  (2)  The  A-V  node  or 
bundle  is  excessively  irritable  at  times  and  the  usual  ideo-ventricular 
rhythm  is  interrupted  by  what  may  be  called  a  nodal  or  bundle 
extrasystole.  On  theoretical  grounds,  one  might  assume  that  such 
a  quickening  of  the  ventricular  activity  would  be  an  event  favor- 
ing an  improved  distribution  of  the  blood.  My  observations  on  this 
patient  were  not  sufficiently  prolonged  to  determine  whether  such 
was  the  case. 

The  graphic  records  of  another  case  of  heart  block  are  pre- 
sented in  Figures  181  and  182.  The  polygraph  shows  a  perfectly 
rhythmic  activity  of  the  auricles  at  a  rate  of  78  and  of  the  ven- 
tricles at  a  rate  of  37,  but  with  a  complete  dissociation  of  the  upper 
and  lower  chambers  of  the  heart.  This  curve  would  suggest  the 
ordinary  type  of  complete  heart  block.  When,  however,  we  come 
to  examine  the  electrocardiographic  record  (Figure  181)  it  presents 
some  unusually  interesting  features.  Here,  again,  there  is  evi- 
dence of  complete  dissociation  of  auricles  and  ventricles.  The  P 
wave  is,  however,  quite  abnormal  in  form.  Instead  of  a  single 
positive  wave,  it  is  diphasic  and  it  is,  therefore,  probable  that  the 
auricular  pacemaker  is  a  point  in  the  muscle  at  a  considerable  dis- 


MIXED  Arrhythmias 


23; 


■^^^1 

n 

9k 

|MH .  -          nl 

R^H^^H 

l9M 

IV 

LS 

1   KREB  Em 

HH9S 

uflml     ^H 

Ira  Bra 

ffSyjPjpfr1 

/'•■.."/■■' 

m 

!5©3fik< 

ipn 

PWI 

ffi^ 

■jBJWj  4  ™J",  ™ 

^■/■lW.1 

iwMwJWjH  ■^^■^^^w^^i 

Jugular 


Brachial 


0.2   scconu 


Figure  179 

Complete   A-V   block.      As   rate  —  86.      Vs    rate  =  30.      Complicated   by   extrasystoles 
c',    c",   c"'.      For   electrocardiogram   of  this   cj.se   see    Figure    iGa. 


F ' 

! 

■ 

1 

.....    i       1      . .  .  .1                      1                          1  ■'". 

Ap        p 

■P 

-■  ■     '           •                                   ■                  '                          ... 

• 

©.2.  £lC9v%cL _ 

Figure  180 

Complete    A-V  block    ?"d    nodal    extrasystoles.      As   rate  =: 
polygram  of  this  case  see  Figure  179. 


5.      Vs   rate  =  30.      For 


z$z  Mixed  Arrhythmias 

tance*  from  the  sino-auricular  node.  Still  more  interesting  is  a 
study  of  the  ventricular  complexes.  These  arc  similar  in  form, 
but  arc  readily  distinguished  from  the  curve  of  a  normal  ven- 
tricular contraction.  The  records  taken  by  leads  I  and  II  (not 
here  reproduced)    showed   ventricular  complexes  of  an  abnormal 

type.      In  lead   1   they  were  directed  upward,  in  lead   II  and  lead    III 

(  Figure  [8i )  they  were  directed  downward.  These  complexes  con- 
form to  the  type  obtained  experimentally  by  Eppinger  and  Roth- 
bergcr,!  through  a  destruction  of  the  left  branch  of  the  bundle  of 
His.  We,  therefore,  conclude  that  in  the  case  under  discussion 
there  existed  a  lesion  dividing  the  main  stem  of  the  A-V  bundle, 
causing  a  dissociation  of  auricular  and  ventricular  activities,  and, 
further,  that  there  was  a  destructive  lesion  in  the  branch  of  the 
A-V  bundle  which  is  distributed  to  the  left  ventricle.  The  ideo- 
ventricular  rhythm,  therefore,  probably  arose,  not  as  is  usual  from 
a  point  in  the  main  stem  of  the  bundle,  but  in  the  right  ventricular 
wall. 

It  is  interesting  to  observe  how  widely  is  distributed  the  prop- 
erty of  rhythmicity  in  the  heart  muscle.  This  heart,  with  a  ven- 
tricular pacemaker  very  remote  from  the  normal  site,  maintained 
an  almost  perfect  rhythmic  activity  over  long  periods  of  time  and, 
on  many  occasions,  when  he  was  under  observation. 

♦Lewis:   Heart,   1910,  ii,  27. 

T/tschr.   f.  klin.   Med.,   1910,  lxx,   1. 


M  [XED   ARRH  y'I  II  Ml  AS 


233 


Figure  181 

Complete    A-V    block    with    destruction    of    the    left    limb    of    the    A-V    bundle.      Note 
diphasic   P  complex.      For  polygram   of  this  case  see   Figure    182. 


.2  second 


Jugular 


Radial 


Figure  182 

Complete    A-V   block.      As    rate=78.      Vs    rate=3^.      For    electrocardiogram    of    this 
case  see   Figure    1S1. 


CHAPTER  XVI 

Position  of  the   Heart   and   Changes  in  the   Disposition   of  the 

Muscle  Mass 

A  discussion  of  changes  in  position  of  the  heart  in  the  chest 
cavity  would  lead  us  outside  of  the  limits  which  we  have  set  to 
the  subject  matter  of  these  pages.  Since,  however,  we  have  laid 
considerable  stress  on  the  use  of  the  electrocardiogram  as  a  means 
of  studying  myocardial  function,  and  have  utilized  not  a  small  por- 
tion of  our  space  in  describing  the  various  characters  of  these  rec- 
ords  and  the  means  for  their  analysis,  it  becomes  necessary  to  ex- 
amine certain  deviations  from  the  usual  type  which  arc  due  to 
changes  in  the  position  of  the  heart  and  which,  therefore,  must 
be  distinguished  from  those  which  are  due  to  intrinsic  myocardial 
alternations. 

The  amplitude  and  direction  of  the  records  obtained  by  the  three 
leads  usually  employed  in  clinical  work  depend  on  the  algebraic 
sum  of  the  currents  developed  in  the  heart  at  any  given  moment, 
but  any  one  of  the  leads  will  record  only  those  currents  which  pass 
in  the  same  plane  as  the  line  connecting  the  points  from  which  the 
particular  lead  is  secured.  Einthoven*  has  shown  that  if  the 
strength  and  direction  of  the  current  developed  by  the  heart  is  rep- 
resented by  a  line  of  given  length  and  direction  the  relative  size 
of  the  deflections  obtained  by  the  three  leads  will  be  proportional 
to  the  projection  of  this  line  on  the  sides  of  an  equilateral  triangle 
whose  sides  represent  the  connections  of  the  points  from  which 
the  current  is  derived  from  the  body.  This  conception  is  illustrated 
in  the  diagram  (Figure  183)  reproduced  by  permission  from  a 
paper  by  Pardee. t  In  this  diagram  the  line  xy  represents  the 
strength  and  direction  of  the  original  current  arising  in  the  heart. 
The  amount  of  current  recorded  in  each  of  the  leads  is  measured 
by  the  projection  of  this  line  on  the  sides  of  the  triangle  formed 
by  connecting  the  points  from  which  the  current  is  led  off.  The 
magnitude  of  the  deflections  of  leads  I,  II  and  III  will  be  pro- 
portional to  the  lines  Xjylt  x..y.  and  .r3ya.     In  the  normal  heart  the 

♦Lancet,  1912,  i,  853. 

tjour.  Amer.  Med.  Assn.,   1914,  lxii,   131 1. 

2  34 


Changes  in   Positn 


III.      I  I  I. API 


Figure  183 

After  Pardee.  Diagram  illustrating-  the  relative  size  of  the  waves  of  the  electro- 
cardiogram in  the  different  leads  obtained  from  a  current  which  is  represented  in  force 
by  the  length  and  in  direction  by  the  position  of  XY. 

RA  right  arm;  LA  left  arm;  L  left  leg.  Roman  numerals  designate  the  leads 
represented   by  the   sides   of   the   triangle. 

■*!  3"l>  -r2  3'2  and  XZ  J'3  indicate  the  relative  amplitudes  of  the  reflections  secured 
from  the  three  leads. 


Figure  184 

After  Pardee.     Diagram  illustrating  the   variations   in   direction   of  the   current  in  the 
different  leads  caused  by  differences  in  direction  of  the  current  developed  in  the  heart. 


236    Changes  in  the  Disposition  of  the  Muscle  Mass 

waves  of  lead  II  arc  larger  than  those  obtained  by  either  lead  1 
or  lead  II.  Einthoven,  Fahr  and  I)e  Waart*  and  Williams f  have 
demonstrated  mathematically  that  reckoned  from  a  fixed  point  in 

the  cardiac  cycle  lead  11  minus  lead  1  equals  had  III.  and  if  two  of 
these  values  are  known  the  third  can  be  correctly  calculated. 

The  direction  of  the  waves  of  a  given  lead  depends  on  the  direc- 
tion of  the  flow  of  the  current  in  the  heart.  This  is  illustrated 
by  the  diagram  (Figure  184),  in  which  the  effect  on  the  direction 
of  the  current  in  the  three  leads,  due  to  a  difference  of  direction  of 
currents  in   the  heart,   is   shown  by  comparison. 

The  most  common  variations  which  one  sees  are  differences  in  the 
relative  amplitude  of  the  deflections  clue  to  changes  in  the  axis  of 
the  heart  caused  by  respiration  or  an  alternation  in  the  position 
of  the  body.  During  inspiration  the  waves  R  and  T  are  smaller 
in  lead  I  and  larger  in  lead  III.  When  the  body  is  turned  from 
the  left  to  the  right  side  there  is  a  deepening  of  the  S  wave  in 
lead  II.  (Irani  has  found  that  the  5"  wave  of  lead  II  was  made 
greater  by  pathological  conditions  (left  pleural  effusions,  etc.)  which 
displaced  the  heart  to  the  right. 

The  records  of  a  case  showing  an  extreme  change  in  the  cardiac- 
axis  is  shown  in  Figures  185,  186,  187,  188,  189  and  190.  The 
patient  had  complete  transposition  of  the  viscera  and  the  heart  was 
on  the  right  side  of  the  chest.  The  records  were  obtained  by  the 
following  leads:  I  =  right  arm  —  left  arm,  II  =  right  arm  —  left 
foot,  III  =  left  arm  —  left  foot,  IV  =  left  arm  —  right  arm, 
V=  left  arm  —  right  foot,  VI  =  right  arm  —  right  foot.  It  is  plain 
that  by  leads  I,  II  and  III  (those  usually  employed)  the  waves  de- 
part from  the  normal  in  direction  and  in  amplitude  in  the  different 
leads.  By  reversing  the  electrodes  (leads  IV,  V  and  VI)  the  elec- 
trocardiogram of  a  normal  heart  is  secured. 

A  one-sided  hypertrophy  of  the  heart  produces  a  change  in  the 
electrical  axis  and,  hence,  a  corresponding  change  in  the  .ural- 
vanometric  records  taken  by  the  three  customary  leads.  This  ob- 
servation was  first  reported  by  Einthoven.l  who  called  attention  to 
the   fact  that  in  many  cases  of  left  hypertrophy  the  R  wave  in 

♦Arch.  f.  d.  ges.  Physiol.,  1913.  cl,  275. 
tAmer.  Jour.   Physiol..   1914,  xxxv.  292. 
JZeitschr.   f.  klin.    Med.,    [909,   lxix,   281. 
Arch.   Internat.  de   Physiol.,   1906,   iv,   132. 


1    '  • 

*V 

.  3 

\ 

:'" 

[iit:  ■■''-.. 

| 

\ 

!       . 

•    £              1 

238    Changes  in  the  Disposition  of  the  Muscle  Mass 

lead   1   was  increased  in  size  and   in  lead    111   was  diminished  or 

even  directed  downward,  while  in  right  hypertrophy  R  was  small 
or  negative  in  lead  1  and  increased  in  amplitude  in  lead  111.  The 
constancy  of  this  phenomenon  has  been  questioned  by  Hering  and 
others  and  a  number  of  apparent  exceptions  have  been  discussed 
in  a  recent  paper  by  Bridgman.f  It  is  probable  that  some  of  the 
discrepancies  in  the  correlation  of  the  heart  condition  and  the 
changes  in  the  electrocardiograms  have  been  due  to  insufficient 
evidence  as  to  the  relative  masses  of  the  right  and  left  chambers 
of  the  heart.  In  a  very  careful  study  of  this  ([notion.  Lewis$  has 
pointed  OUt  that  the  usual  methods  of  examination  are  quite  in- 
sufficient to  determine  the  relative  degrees  of  hypertrophy  of  the 
right  and  left  ventricles.  As  a  rule,  he  found  that  his  cases  of 
mitral  and  pnlmonary  stenosis,  with  clinical  evidence  of  right-sided 
hypertrophy,  showed  the  characteristic  electrocardiograms  of  right 
hypertrophy,  as  indicated  by  Einthoven,  while  cases  of  hypertension 
and  aortic  insufficiency,  with  signs  of  left  hypertrophy,  showed  the 
graphic  evidence  ascribed  to  left  hypertrophy.  There  were,  how- 
ever, a  number  of  discrepancies  and  these  he  explains  on  the 
ground  that  the  clinical  evidence  of  right  or  left  hypertrophy  was 
not  conclusive.  In  a  small  number  of  cases,  which  he  was  able 
to  study  by  separating  the  chambers  by  dissection  and  taking  their 
weights  he  was  able  to  show  that  the  electrocardiographic  records 
corresponded  to  the  degree  of  preponderance  of  the  right  or  the 
left  heart. 

Fraser*  produced  experimental  right  and  left  hypertrophy  in  rab- 
bits by  the  injection  of  adrenalin,  spartein  and  bacterial  toxins,  and 
was  able  to  show  a  correlation  between  the  changes  in  the  elec- 
trocardiograms and  careful  post-mortem  examinations. 

It  seems  to  me  that  the  evidence  is  reasonably  conclusive  that 
right  ventricular  predominance  is  characterized  by  a  diminution  in 
the  size  of  R  and  a  deepening  of  6"  in  lead  I,  an  increase  in  R  and 
a  lessening  of  .V  in  lead  111,  while  left  ventricular  predominance  is 
shown  by  an  increase  in  the  amplitude  of  R  and  a  decrease  in  5* 
in  lead  I,  and  a  shortening  of  R  and  a  deepening  of  S  in  lead  III. 

fArch.   Int.   Med.,   1915,  xv,  487. 

tlleart,   1914.  v,  367. 

*Jour.  Exp.  Med.,   191 5,  xxii,  292. 


-3V 


240     Changes  [N  the  Disposition"  of  the  Muscle  Mass 

A  comparison  of  the  records  obtained  in  right  and  left  ventricular 
predominance  are  shown  on  pages  239  and  _•  \  1 .  Figures  mi .  192  and 

[93  were  secured  from  a  ease  of  long-standing  hypertension  ( -'-'5- 
260  mm.  Hg.),  with  physical  signs  and  radiographic  evidences  of 
marked  left  ventricular  hypertrophy.  Figures  104,  i<)5  and  196 
are  from  a  patient  with  mitral  stenosis  and  clinical  and  radio- 
graphic evidences  of    right-sided   hypertrophy. 

Lewis  has  called  attention  to  the  fact  that  infants  under  three 
months  of  age  show  an  electrocardiogram  of  the  right  ventricular 
hypertrophy  type  which  gradually  changes  to  the  normal  type. 


"Sf 

I 

i 

n  11 

1 

111 

i 

II 

Hi            J 

H 

III 

illitlllllttlllri 

mil-    ' 

o  — 

fa  '5 


24 1 


fa  5 


fM^HHlfH-n 


■  ■      »■..;..:.:    .::■!:,.!. 


CHAPTER  XVII 

Treatment 
GENERAL    PRINCIPLES 

The  object  of  the  treatment  of  myocardial  disease  is  the  restora- 
tion of  function.  This  may  be  accomplished  by  (  i  )  the  removal 
of  an  abnormal  structural  condition  of  the  heart  muscle,  or,  fail- 
ing this,  (2)  maintaining  a  proper  relation  between  the  amount  of 

work   performed   by   the   heart   and   its    functional   capacity. 

Functional  abnormalities  are  usually  the  result  of  organic  struc- 
tural changes;  there  is  little  question  that  we  can  correct  these 
to  some  extent  and  possibly  in  certain  instances  restore  the  muscle 
cell  to  the  normal.  In  other  instances  the  functional  derangement 
is  dependent  on  chemical  rather  than  histological  changes  in  the 
muscle  cells  or  nerve  endings,  these  too  are  often  capable  of  com- 
plete correction. 

An  adequate  circulation  may  be  secured  by  improving  the  con- 
dition of  the  heart  itself,  or  by  reducing  the  demands  on  the  heart 
to  a  point  where  a  defective  myocardium  may  still  be  able  to  per- 
form  the   necessary   work. 

It  is  obvious  that  etiological  studies  are  of  vital  importance  in 
determining  the  means  suitable  to  be  employed  in  the  removal  of 
the  particular  lesion.  For  example,  the  acute  infections,  rheuma- 
tism and  syphilis,  each  present  their  individual  problems  and  a 
corresponding  solution. 

Taken  in  hand  in  the  early  stages,  myocardial  changes  due  to 
such  toxins  may  often  be  repaired  and  frequently  complete  restora- 
tion of  function  may  be  attained.  However,  as  we  know  only  too 
well  our  early  efforts  to  avert  fixed  structural  changes  are  all  too 
frequently  unavailing.  Diphtheria  has  left  behind  degenerative 
changes,  the  active  inflammatory  reaction  of  rheumatism  has  sub- 
sided, but  the  bands  of  fibrous  tissue  separating  or  replacing  muscle 
cells  remain.  An  active  syphilitic  process  may  have  been  controlled, 
but  the  gumma  may  be  replaced  by  scar  tissue  interrupting  the 
continuity  of  functionally  active  myocardial  tissue  or  may  have 
produced  changes  in  the  walls  of  the  blood  vessels  materially  affect- 


Trkatmknt  243 

ing  the  nutrition  of  otherwise  healthy  contractile  areas.  Advancing 
years   have   brought   with   them   blood    vessels   atheromatous   and 

studded  with  calcareous  deposits  and  tin-  elasticity  of  their  walls 
is  all  hut  gone.  The  outside  demands  of  excessive  physical  exer- 
tion of  the  contracted  kidney  or  of  a  general  arteriosclerosis  have 
left  in  their  train  dilated  cardiac  chambers  with  the  myocardium 
over-stretched  or  thickened.  The  recognition  of  such  structural 
changes  demands  that  we  meet  the  problem  by  a  different  method 
and  by  new  agencies.  Though  we  frankly  admit  that  we  cannot 
dissolve  calcareous  deposits  or  replace  connective  tissue  with  new 
muscle  cells,  we  have  by  no  means  exhausted  our  opportunities  of 
service  to  our  patient.  There  are  at  our  disposal  a  number  of 
measures  which  may  help  to  improve  the  myocardium  and  an  even 
greater  number  through  which  we  may  influence  the  demands  on 
the  heart  and  thus  limit  the  stress  to  the  capabilities  of  the  organ 
damaged  beyond  possibilities  of  restoration  to  the  normal. 

INDIVIDUALIZATION 

Success  in  the  treatment  of  myocardial  disease  is  primarily  de- 
pendent upon  individualization.  It  is  in  this  sphere  that  the  newer 
methods  of  investigating  the  myocardium,  to  which  such  a  con- 
siderable portion  of  this  book  has  been  devoted,  are  of  greatest 
value.  Up  to  the  present  time  these  studies  have  been  in  a  large 
measure  directed  to  discovering  the  nature  of  the  abnormal  func- 
tion and  in  designating  in  each  instance  the  fundamental  property 
of  the  muscle  cell  which  is  at  fault.  Thus  we  are  able  to  say 
with  considerable  certainty  that  in  one  case  a  defect  in  conduc- 
tivity, in  another  abnormal  irritability  and  in  a  third  a  change  in 
contractility,  is  primarily  the  basis  of  the  functional  change.  The 
effect  of  drugs  and  other  remedial  measures  on  these  fundamental 
functions  of  cardiac  tissue  have  been  less  completely  investigated, 
but  such  studies  as  have  been  made  have  already  furnished  infor- 
mation of  great  value  in  determining  the  mode  of  their  activities 
and  in  pointing  the  way  to  their  employment  in  abnormal  func- 
tional states.  It  is  needless  to  suggest  that  further  research  along 
these  lines  is  most  desirable  and  should  be  a  fruitful  source  of 
information.  It  should  serve  to  extend  our  knowledge  in  a  very 
useful  field  and  to  correct  many  of  the  notions  now  in  vogue  in 


J44  Treatment 

regard  to  the  treatment  and  management  of  those  suffering  from 
diseases  of  the  heart 

REST 

The  most  important  single  measure  at  our  command  in  the  treat- 
ment of  diseases  of  the  heart  is  a  curtailing  of  the  work  that  the 
heart  is  called  upon  to  perform.  This  does  not  mean  that  every 
case  showing  a  defect  of  myocardial  function  needs  rest,  and  it 
is  one  of  the  important  duties  of  the  physician  to  determine  in 
each  instance  whether  the  demands  on  tin-  myocardium  are  too 
great  and  if  so  to  what  degree  they  should  he  modified. 

When  the  body  is  at  rest,  the  heart  liberates  only  a  small  part 
of  the  force  of  which  it  is  capable;  the  remainder  is  called  the 
"reserve  force."  This  factor  of  safety  is  very  considerable  in  the 
normal  heart  and  it  has  heen  estimated*  that  the  reserve  force 
of  the  heart  renders  it  ahle  to  perform  thirteen  times  the  amount 
of  work  which  it  accomplishes  when  the  hody  is  at  rest.  A  mod- 
erate amount  of  physical  exertion  calls  upon  the  heart  for  the 
expenditure  of  four  times  as  much  work  as  is  required  in  a  state 
of  bodily  inactivity,  hut  the  normal  heart  will  readily  perform  this 
task  year  after  year  if  its  work  is  alternated  with  proper  intervals 
of  rest. 

The  insufficient  heart  is  one  in  which  the  "reserve  force"  is  below 
the  normal.  The  depletion  of  the  reserve  may  have  been  due  to 
excessive  demands  on  a  normal  heart  or  normal  demands  which 
cannot  he  met  by  a  damaged  heart.  It  is  evident  that  the  term 
"insufficient  heart"  is  a  relative  one.  The  exhaustion  of  reserve 
strength  may  be  very  slight  or  of  a  degree  that  is  barely  com- 
patible with  life.  When  the  heart  is  insufficient  and  the  reserve 
force  is  depleted  to  a  marked  degree,  rest  is  always  indicated. 

The  first  object  attained  by  bodily  rest  is  a  diminished  demand 
on  the  heart  for  work,  i.e.,  the  drain  on  the  reserve  force  is  cur- 
tailed. Important  as  is  this  factor,  there  are  other  associated  bene- 
fits which  should  not  be  lost  sight  of  in  reckoning  the  value  of 
this  mode  of  treatment.  Physical  inactivity  usually  entails  a  slow- 
ing of  the  heart.  This  is  brought  about  by  reflex  nervous  influ- 
ences affecting  the  pacemaker.  In  a  normal  heart  beating  at  a 
rate  of   70,  the  cardiac   cycle   occupies  0.862   second.      In   such   a 

*Lewy:  Ztschr.  f.  klin.  Med.,  1896-97,  xxxi,  320. 


Treatment  245 

heart  Edgren  has  estimated  that  duration  of  systole  is  0.379  sec~ 
ond,  diastole  0.483  second  and  the  time  occupied  in  diastole  in  a 
twenty-four  hour  period  is,  therefore,  over  thirteen  hours.  In  the 
accelerated  heart  the  shortening  of  the  cycle  is  almost  entirely  at 
the  expense  of  the  diastolic  period,  the  length  of  systole  remaining 
practically  unchanged.  In  a  heart  heating  140  per  minute,  the  total 
time  occupied  hy  diastole  in  twenty-four  hours  is  reduced  to  less 
than  four  hours.  The  diastolic  period  is  the  time  in  which  the 
myocardium  obtains  its  rest  and  the  above  figures  sufficiently  in- 
dicate the  great  variations  in  this  period  of  recuperation  with 
different  heart  rates.  During  diastole  the  molecules  are  built  up, 
upon  which  depend  the  fundamental  properties  of  the  muscle  cell, 
and,  other  things  being  equal,  the  longer  this  period  of  recovery 
the  more  mature  will  be  these  molecules  and  the  more  effective  their 
dissociation  during  systole.  Thus  the  contractile  power  of  the 
muscle  cell  is  proportional  to  the  period  of  rest  preceding  its  utiliza- 
tion. The  above  is  illustrative  of  the  advantage  to  the  heart  of 
conditions  permitting  the  fundamental  properties  of  the  muscle  cell 
to  reach  their  optimum  during  each  cycle,  and  for  this  physical 
rest  is  one  of  our  most  useful  agents. 

Another  important  benefit  to  the  muscle  cell  attained  by  pro- 
longing its  period  of  rest  is  dependent  on  the  fact  that  the  myo- 
cardium receives  its  nutrient  supply  of  blood  during  diastole ;  it, 
therefore,  follows  that  a  lengthening  of  an  abnormally  short  dias- 
tolic period  affords  a  better  opportunity  for  the  muscle  cells  to 
receive  their  full  quota  of  nutrient  material,  upon  which  must 
depend  a  normal  functional  activity  and  the  storing  of  an  adequate 
reserve. 

The  development  of  cardiac  hypertrophy,  so  desirable  in  many 
cases,  is  dependent  on  an  adequate  blood  supply,  which  can  best 
be  secured  by  prolonging  the  diastolic  period. 

The  question  may  now  be  asked  in  what  patients,  the  subjects 

of  abnormal  myocardial   function,  is  rest*  indicated  and  to  what 

degree  must  it  be  employed?     To  such  a  question  no  categorical 

answer  can  be  given,  but  a  few  suggestions  will  be  offered  which 

may  help  the  physician  in  formulating  the  policy  suited  to  the  needs 

of  the  individual  case. 

*We  would  define  "rest."  as  used  in  the  present  discussion,  as  any  curtail- 
ment of  the  physical  activity  to  which  the  individual  is  accustomed. 


246  Treatment 

rhe  object  to  be  attained  is  to  prevail  myocardial  damage  or, 
if  this  is  in  process,  to  limit  its  extent;  to  maintain  a  normal  dis- 
tribution of  the  blood  throughout  the  body,  and  to  accomplish  this 
without  permanently  reducing  the  reserve  force,  or,  it'  the  reserve 

force  is  already  curtailed,  to  afford  an  opportunity  for  its  restitution. 
Absolute  rest  in  bed  is  advisable  in  all  eases  where  an  active  in- 
fective process  is  localized  in  the  heart  substance  and  in  the  active 
stages  <>i  all  infectious  diseases,  the  toxins  of  which  are  prone  to 

attack  the  cardiac  tissues.  It  is  also  indicated  in  the  early  Stages 
for  a  heart  which  has  become  insufficient  from  any  cause  what- 
ever, the  insufficiency  being  suggested  by  a  greater  or  less  degree 

of  dyspnoea  and  other  evidences  of  improper  blood  distribution. 
Frequently,  when  the  reserve  force  of  a  heart  is  only  moderately 
depleted,  a  period  of  confinement  to  bed,  while  sometimes  not 
absolutely  necessary,  will  allow  the  patient  to  shorten  materially  the 

time  required  to  recover  his  balance.  In  cases  of  acute  or  chronic 
severe  cardiac  insufficiency,  with  complete  exhaustion  of  reserve 
force,  absolute  rest  in  bed  is  imperative. 

Many  mild  infections  and  febrile  conditions,  such  as  bronchitis, 
indigestion,  diarrhoea,  etc.,  not  ordinarily  considered  of  serious  im- 
port, attain  a  new  significance  when  they  occur  in  a  subject  with 
a  weak  cardiac  muscle;  such  patients  should  be  confined  to  bed 
until  the  complication  has  cleared  up. 

Few  patients  with  extreme  myocardial  insufficiency  can  he  kept 
flat  in  bed  and  some  are  far  more  comfortable  and  will  improve 
quite  as  rapidly  if  they  are  allowed  to  spend  all  their  time  in  a 
chair. 

The  length  of  time  that  a  patient  should  remain  in  bed  is  often 
rather  a  difficult  matter  to  decide.  I  think  the  more  common  error 
is  to  allow  the  patient  up  too  soon,  but  in  a  certain  number  the 
confinement  to  bed  may  be  overdone  and  there  is  a  more  rapid 
improvement  if  the  heart  is  given  the  extra  work  which  the  change 
in  position  entails.  The  patient  should  he  confined  to  bed  until 
it  i-  quite  evident  that  the  extreme  insufficiency  has  disappeared 
and  until  he  has  accumulated  enough  reserve  force  to  change  his 
position  and  make  certain  simple  movements  without  inducing  symp- 
toms of  exhaustion  of  the  reserve  force.  Changes  to  an  upright 
position  and  the  transition  to  walking  and   other  exercises  should 


Treatment  247 

be  very  gradual  and  should  depend  on  a  study  of  tin-  reaction  of 
each  individual  to  the  work  thus  newly  imposed.     All  advance 
should  be  made  only   under   the   explicit   written   directions   of    the 
physician. 

Many  cases  of  mild  chronic  myocardial  insufficiency  do  not  need 
to  go  to  bed,  limitation  of  their  usual  physical  activities,  change 
in  occupation  and  definite  periods  of  enforced  inactivity  are  suffi- 
cient to  allow  the  heart  to  recover  a  reasonable  amount  of  res< 
force.  In  arranging  a  program  for  each  patient,  the  ingenuity  of 
the  physician  will  often  be  greatly  taxed.  Our  prescription  must 
be  one  which  the  patient  can  follow.  If  merely  correct  in  theory, 
but  impossible  of  accomplishment,  it  will  be  as  little  creditable  to 
the  sagacity  of  the  physician  as  it  is  of  benefit  to  the  patient.  We 
can  do  better  than  to  advise  a  poor  man,  who  has  to  climb  three 
flights  to  his  two-room  tenement,  to  install  an  elevator.  A  tem- 
porary interruption  or  a  change  of  occupation  may  be  imperative, 
but  the  psychological,  as  well  as  the  physical,  effect  on  the  patient 
must  be  carefully  considered  before  this  is  advised. 

Our  discussion  has  hitherto  contemplated  conditions  in  which 
myocardial  defects  are  associated  with  cardiac  insufficiency.  There 
are  a  vast  number  of  patients  with  disorders  of  myocardial  func- 
tion, some  undoubtedly  due  to  real  organic  changes,  who  show 
no  evidence  of  cardiac  insufficiency.  In  the  majority  of  these  rest 
is  not  indicated,  indeed  they  are  better  oft  following  their  usual 
mode  of  life,  provided  this  does  not  involve  excessive  physical 
exertion,  rather  than  modifying  this  and  thus  introducing  a  con- 
tinuous state  of  introspection  which  may  ultimately  unfit  them  for 
both  the  work  and  the  pleasures  of  life.  There  are  a  certain  num- 
ber, however,  whose  activities  should  be  curtailed,  at  least  for  a 
temporary  period,  with  the  object  of  warding  off  a  subsequent  con- 
dition of  exhaustion  of  the  reserve  force  or  of  correcting  a  func- 
tional derangement  which  is  a  source  of  apprehension  to  the  patient, 
or  his  friends.  Such  individuals  are  greatly  helped  if  we  can  as- 
sure them  that  the  course  of  treatment  is  temporary  and  for  the 
purpose  of  bringing  about  a  complete  restoration  of  the  normal 
cardiac  functions.  It  is  the  duty  of  the  physician  to  sift  care- 
fully these  cases,  using  all  the  facilities  which  modern  methods 
have  placed  at  his  disposal,  and,  backed  by  the  evidence  thus  ob- 


24S  Treatment 

tained,  assist  his  patient  l>v  advising  a  mode  of  life  suited  to  the 
individual  conditions. 

Fear  and  apprehension  arc  very  Frequent  accompaniments  of  myo- 
cardial disorders.  The  most  potent  influence  that  can  be  employed 
in  correcting  such  psychological  states  is  the  kindly  but  firm  as- 
surance, based  on  real  knowledge,  given  by  the  physician  to  the 

patient.  Mental  rest  is,  to  some  patients,  as  important  as  physical 
rest.  Worry  and  excitement,  acting  retlcxly  through  the  extra- 
cardial  nerves,  accelerate  the  heart  or  exert  their  influence  un- 
evenly, rendering  an  irritable  heart  less  able  to  preserve  its  rhyth- 
mic activity  and  thus  reducing  its  efficiency.  The  method  to  he 
employed  to  combat  such  conditions  again  calls  for  the  most  pains- 
taking efforts  of  the  medical  adviser  in  offering  advice  suited  to  the 
individual.  Withdrawal  from  business  or  other  usual  occupations 
will,  in  many  cases,  augment  rather  than  relieve  nervous  tension. 
Change  of  surroundings  and  mild,  suitable  diversions  may  serve 
our  purpose  in  one  case  and  utterly  fail  in  another.  Hence,  the 
study  of  the  psychology  of  each  individual  becomes  an  important 
part  of  the  physician's  duty. 

In  other  portions  of  this  book  the  significance  of  special  dis- 
orders and  the  amount  of  rest  suited  to  each  is  discussed. 

EXERCISE 

The  indications  for  and  method  of  transition  from  a  state  o\ 
complete  bodily  rest  to  movements  requiring  moderate  muscular 
exertion  have  been  touched  upon  in  connection  with  the  discus- 
sion of  rest.  It  remains  for  us  to  consider  the  advantages  which 
may  be  secured  by  exercise,  the  class  of  cases  upon  which  regu- 
lated activities  have  a  favorable  effect  and  the  methods  which  should 
be  utilized  in  applying  this  form  of  treatment. 

The  most  evident  effects  of  moderate  exercise  on  a  normal  heart 
are  an  immediate  increase  in  rate  and  the  blood  pressure.  If  the 
exercise  has  not  overtaxed  the  heart,  its  rate  and  the  blood  pres- 
sure will  return  to  normal  a  few  minutes  after  the  cessation  of  the 
exercise.  In  general,  the  insufficient  heart  reacts  to  exercise  in  the 
same  manner  as  the  normal  heart,  provided  that  it  too  is  not  over- 
taxed. In  order  that  a  heart  may  not  be  overtaxed,  the  demands 
put  upon  it  must  fall  below  its  maximal  working  capacity,  which 
consists  of   the  sum  of  the   force  necessary  to  carry  on  the  cir- 


Treatmeni  249 

dilation  while  the  body  is  at  rest  rind  its  reserve  force.  The  dif- 
ference in  the  working  capacity  of  the  normal  and  the  insufficient 
heart  is  a  difference  in  the  amount  of  reserve  force. 

There  is  no  advantage  to  an  insufficient  heart  in  the  increase  of 
rate  produced  by  exercise,  but  if  the  acceleration  is  not  excessive 
and  the  period  of  its  duration  is  brief,  it  usually  has  no  detrimental 
effect.  T1k  heightened  blood  pressure  in  the  first  part  of  the  aorta 
increases  the  amount  of  blood  passing  through  the  coronaries,  and 
this  furnishes  more  nutritive  material  to  the  myocardium.  As  a 
result  of  this,  the  individual  muscle  fibers  become  larger*  and 
actually  increase  in  number.f  Hence,  there  is  a  thickening  of  the 
musculature  which  we  recognize  as  hypertrophy  of  the  heart. 
Exercise  increases  the  work  of  the  heart.  The  heart  reacts  to  this 
increased  work  with  hypertrophy.  Hypertrophy  means,  at  least 
for  a  time,  an  increased  reserve  force.  Aside  from  the  direct 
effect  on  the  myocardium,  exercise  facilitates  the  return  flow  of 
the  blood  from  the  extremities  and  reduces  the  work  of  the  heart 
ordinarily  expended  in  this  direction,  while  at  the  same  time  there 
is  an  increased  flow  of  blood  to  the  right  side  of  the  heart. 

A  discussion  of  the  benefits  to  the  patients  from  exercise  other 
than  those  directly  affecting  the  circulatory  apparatus  are  beyond 
the  scope  of  the  present  papers.  But  such  items  as  the  relief  of 
congestion  of  the  various  organs  of  the  body,  the  improvement 
in  appetite  and  digestion,  the  betterment  of  the  excretory  activities 
of  bowel,  kidneys  and  skin,  the  betterment  of  respiratory  condi- 
tions, etc.,  etc.,  should  not  be  forgotten  in  estimating  the  value  of 
this  form  of  therapeutics. 

In  considering  the  classes  of  patients  who  may  be  benefited  bv 
a  course  of  graded  exercises,  it  may  be  well  first  of  all  to  enu- 
merate those  in  which  any  measures  of  this  kind  are  absolutely 
contraindicated : 

1.  Acute  infectious  diseases  in  which  a  myocardial  involvement 
has  commenced  or  may  be  apprehended. 

2.  Acute  dilatation  after  overexertion. 

3.  A  heart  which  is  not  compensated  during  complete  bodily  rest. 

4.  Angina  pectoris. 

♦Goldenburg:  Virchows  Arch.,  1886,  ciii,  88. 
fZielenko :  Ibid.,  1875,  lxii,  29. 


250  Treatment 

5.   Cardiac  asthma. 
<>.   Chronic  nephritis. 

7.  General  arteriosclerosis  with  high  blood  pressure. 
Among  those  to  whom  we  may  be  confident  thai   properly  reg- 
ulated exercises  will  be  of  benefit,  arc: 

1.  Young  people  with  disproportionate  small  hearts.  We  see  this 
condition  not  infrequently  in  young  persons  who  have  grown  rap- 
idly, but  whoso  cardiac  development  has  apparently  failed  to  keep 
pace  with  the  vest  of  the  body.  It  occurs  not  only  in  those  of 
sedentary  habits,  but  also  in  boys  who  are  exercising  vigorously. 
These  may  show  signs  of  cardiac  insufficiency  of  a  mild  grade, 
with  no  discoverable  abnormality  other  than  a  myocardium  that 
is  relatively  small.  These  patients  should  not  be  deprived  of  their 
exercise,  but  for  their  irregular  and  often  too  violent  activities  a 
course  of  regular  and  carefully  graded  training  should  be  substituted. 

2.  Those  of  sedentary  habits  whose  cardiac  tissues  are  sufficient 
in  quantity;  but  deficient  in  quality.  Here  exercise  acts  as  a  direct 
stimulant  to  cardiac  metabolism  and  the  results  of  its  employment 
are  most  gratifying. 

3.  Young  persons  with  sinus  arrhythmia.  The  instability  of  the 
pacemaker  and  its  sensitiveness  to  reflex  nervous  influences,  are 
often   favorably  affected  by  properly  controlled  exercise. 

4.  (  >bese  patients  in  whom  the  cardiac  reserve  is  not  sufficient 
to  support  the  extra  burden  of  overweight.  In  these  a  strict  dietary 
should  play  an  important  part.  In  the  very  aged,  or  when  arterio- 
sclerosis is  present,  exercise  should  be  used  with  great  caution. 

Lying  midway  between  the  group  in  which  exercise  is  distinctly 
contraindicated  and  the  group  in  which  we  may  invariably  expect 
favorable  results  from  its  employment,  art'  many  cases  in  which 
the  results  of  exercise  cannot  be  as  confidently  predicted.  We 
should  always  individualize,  but  in  the  cases  under  consideration  a 
minute  study  of  each  patient's  condition  and  his  reaction  to  exer- 
cise is  particularly  required. 

For  the  most  part,  these  arc  patients  wdio  are  convalescing  from 
an  acute  myocardial  process  or  chronic  cases  whose  hearts  have 
become  decompensated;  all  of  them  show  a  greater  or  less  impair- 
ment of  reserve  force  and  a  period  of  rest  must  precede  any  meas- 
ures directed  toward   increasing  the   work   of  the  heart.     This  is 


Treatment  251 

especially  the  case  in  those  in  whom  the  reserve  force  has  been 
depleted  hy  physical  exertion  which  has  exceeded  the  maximal  work- 
ing capacity  of  the  heart.  After  a  period  of  rest,  during  which 
the  heart  will  have  had  an  opportunity  of  adding  something  to  its 

reserve  force,  massage  or  the  mildest  forms  of  resistance  move- 
ments may  he  tried  for  brief  periods;  if  the  reaction  of  the  patient 
to  these  mild  procedures  is  favorable,  they  may  he  continued  and 
gradually  increased  in  the  manner  indicated  below.  If,  however, 
the  cardiac  response  is  bad,  rest  must  he  continued  and  all  forms 
of  activity  deferred  to  a  subsequent  and  more  propitious  occasion. 

The  chief  advantages  of  the  introduction  of  a  course  of  graded 
exercises  are  that  both  passive  and  active  movements  of  this  kind 
can  be  more  accurately  measured  than  in  the  case  of  voluntary 
indiscriminate  activities,  which  the  patient  will  undertake  when  not 
under  close  supervision.  Progress  is  more  uniform  and  con- 
valescence is  less  apt  to  be  interrupted  by  frequent  temporary  set- 
backs due  to  thoughtless  excessive  demands  on  the  reserve  force, 
and  is  therefore  shortened. 

In  order  that  the  patient  may  receive  benefit  from  this  form  of 
treatment,  it  must  be  conducted  under  the  closest  supervision  of 
the  physician.  The  physician  must  either  carry  out  the  treatment 
in  person  or  must  be  present  during  each  of  the  earlier  treatments 
and  at  intervals  during  the  later  stages,  in  order  that  he  may 
observe  the  patient's  reaction  and  advise  as  to  the  rapidity  witli 
which  advances  shall  be  made.  When  the  effect  of  treatment  is 
established,  the  physician  may  by  degrees  avail  himself  of  the  assist- 
ance of  a  trained  attendant  always  working  under  his  direction. 
On  a  number  of  occasions  I  have  seen  considerable  harm  as  the 
result  of  the  well-meaning,  but  injudicious,  efforts  of  an  attendant 
ignorant  of  the  limits  which  should  be  imposed. 

The  physician  must  prescribe  the  kind  of  exercise,  the  length 
of  treatment  and  the  intervals  of  rest  in  each  instance  and  vary 
these  in  accordance  with  the  changes  in  the  reserve  force.  The 
physician  is  guided  in  measuring  the  amount  of  exercise  desirable 
by  the  reaction  of  the  patient.  This  does  not  mean  the  subjective 
sensations  of  the  patient,  as  these  are  often  misleading.  The  best 
guides  are  a  study  of  the  pulse  rate  and  blood  pressure.  One  can- 
not lay  down  actual  figures,  but  the  increase  in  pulse  rate  during 


2  5-  Treatment 

the  exercise  should  never  be  excessive.  A  good  reaction,  as  indi- 
cated by  the  pulse  rate,  is  one  in  which  the  rate  increases  during 
exercise  (not  over  20  beats  per  minute)  and  returns  to  the  pre- 
exercise  rate  or  below  this  within  3  minutes  after  the  cessation  of 

the  exercise.  Systolic  blood  pressure  should  show  a  maximum  in- 
crease on  the  completion  of  the  exercise.  If  the  pressure  rise  is 
prolonged  after  the  pulse  rate  begins  to  decline,  it  indicates  that 
the  work  to  which  the  myocardium  has  been  subjected  is  excessive. 

The  most  important  principle  to  be  observed  in  planning  a  course 
of  graded  exercises  is  to  regulate  the  demands  on  the  heart  so 
that  they  shall  never  exceed  its  reserve  force.  If  the  treatment 
is  commenced  very  early,  that  is,  before  the  patient  is  allowed  out 
of  bed,  or  even  when  he  is  beginning  to  sit  up,  at  a  time  when 
the  reserve  force  is  still  small,  a  start  should  be  made  with  gentle 
massage  of  the  extremities,  always  working  from  the  periphery 
toward  the  trunk.  Short  periods  of  massage  (10  minutes)  should 
alternate  with  ten-minute  periods  of  rest,  and  the  whole  treatment 
should  not  consume  more  than  half  an  hour.  As  the  reserve  force 
increases,  the  massage  may  include  the  whole  body.  The  periods 
of  rest  may  be  shortened  and  the  duration  of  treatment  lengthened, 
but  it  should  never  exceed  one  hour.  Following  the  course  of 
massage,  passive  exercises  may  be  introduced.  Here  the  patient 
relaxes  completely  and  his  extremities  are  gently  moved  by  the 
attendant.  Next  are  added  simple  voluntary  movements  made  by 
the  patient  at  first  slowly  without  resistance,  later  more  rapidly 
and  against  resistance  furnished  by  the  attendant.  This  may,  in 
turn,  be  followed  by  exercises  involving  self-resistance,  in  which 
certain  muscles  are  contracted  by  a  voluntary  effort  against  resist- 
ance introduced  by  opposing  sets  of  muscles  (e.g.,  the  patient  imag- 
ines he  is  lifting  a  weight  with  one  hand,  etc.,  etc.). 

All  these  exercises  should  be  employed  for  short  intervals  only, 
alternating  with  periods  of  rest,  and  a  period  of  complete  relaxa- 
tion in  the  horizontal  position  for  half  an  hour  or  more  should 
follow  each  treatment. 

Along  with  these  exercises  the  patient  should  be  taught  the  proper 
method  of  breathing,  a  very  important  element  in  facilitating  blood 
flow. 

Patients  with  a  fair  amount  of  reserve  force  should  be  allowed 


Treatment  253 

to  walk  short-measured  distances  on  the  level,  later  the  distant  e 

may  be  increased  and  climbing  may  be  tried.  The  changes  should 
be  very  gradual  and  always  controlled  by  a  study  of  the  effect  which 
the  prescribed  exercise  produces.  A  patient  with  a  permanently 
damaged  heart  must  be  taught  that  there  arc  definite  limits  to  the 
stress  with  which  his  heart  can  definitely  cope,  and  he  must  learn 
to  live  within  these  limits  or  pay  the  penalty.  What  the  limits 
may  be  can  only  be  determined  by  a  careful  study  of  the  indi- 
vidual. The  degree  to  which  some  patients  with  severe  grades  of 
myocardial  insufficiency  can  improve  is  extraordinary.  They  may 
reach  a  point  where  they  can  do  a  surprising  amount  of  heavy 
manual  labor  with  impunity. 

In  selecting  the  form  of  exercise  suitable  for  a  patient  whose 
heart  has  attained  a  fair  degree  of  strength,  it  is  often  helpful  to 
ascertain  the  kind  of  exercise  in  which  he  is  proficient.  On  the 
links  a  trained  golfer  will  make  much  less  demand  on  his  reserve 
than  the  beginner,  even  riding  may  be  permissible  for  a  skilled 
horseman. 

It  has  been  our  purpose  to  outline  the  principles  involved  in  ap- 
plying systematic  graded  exercises,  the  details  of  the  various  meth- 
ods as  advocated  by  Herz  and  Zander,  Oertel's  Terrain  cure, 
Schott's  modification  of  the  Swedish  movements  as  used  at  Nau- 
heim,  Barringers  dumbbell  exercises,  etc.,  etc.,  are  best  studied  in 
the  original  papers  or  in  special  treatises  devoted  to  these  subjects. 

BLOOD-LETTING 

Under  ordinary  conditions,  the  hydrostatic  pressure  in  the  vas- 
cular system  tends  to  make  the  blood  in  the  veins  rise  to  the  same 
heights  as  in  the  arteries.  The  force  of  the  heart,  assisted  by  the 
suction  action  of  respiration  and  the  muscular  pressure  on  the  veins, 
returns  the  blood  to  the  heart  at  the  same  rate  at  which  it  is 
sent  out.  A  prominent  feature  of  many  cases  of  cardiac  insuffi- 
ciency is  an  abnormal  distribution  of  the  blood.  A  weak  myo- 
cardium, with  loss  of  muscular  tone,  predisposes  the  cardiac 
chambers  to  dilatation  ;  when  the  right  ventricle  is  thus  affected 
and  tricuspid  insufficiency  ensues,  the  back  pressure  leads  to  an 
overfilling  of  the  veins  and  right  heart.  It  is  under  these  condi- 
tions that  bleeding:  is  often  of  great  value.     The   volume  of  the 


254  Treatment 

blood  brought  to  the  heart  is  reduced  and  the  embarrassment  of 
the  right  heart  is  at  leasl   temporarily  relieved. 

Venesection  lias  an  effeel  thai  is  essentially  mechanical.  It  de- 
creases the  amount  of  blood  brought  to  the  right  ventricle,  hence 
this  contracts  more  completely  and  more  efficiently  and  forces  more 
blood  into  the  left  heart,  which,  in  turn,  sends  more  blood  into 
the  aorta.  This  increases  arterial  pressure  and,  incidentally,  the 
blood  flow  in  the  coronaries,  thus  improving  the  nutrition  of  the 
myocardium. 

The  indications  for  venesection  arc  an  overdistended  right  heart 
and  venous  engorgement  in  a  patient  whose  condition  demands 
prompt  interference,  where  there  is  no  time  to  wait  for  the  action 
of  drugs  or  other  remedial  measures  or  where  these  have  failed. 
The  procedure  will  often  afford  a  respite  during  which  other  meas- 
ures may  have  an  opportunity  to  act. 

I  deeding  is  best  accomplished  by  opening  a  superficial  vein  at 
the  bend  of  the  elbow  after  applying  to  the  upper  arm  a  bandage 
sufficiently  snug  to  obstruct  the  venous  return.  By  puncturing  the 
vein  with  a  good-sized  aspirating  needle,  to  which  is  attached  a 
rubber  tube  leading  to  a  flask,  much  of  the  disorder  incident  to  the 
cruder  methods  may  be  avoided.  The  blood  flow  may  be  facili- 
tated by  gentle  mouth  suction  by  the  operator  on  another  tube  lead- 
ing from  the  flask.  The  blood  flow  is  also  increased  by  getting  the 
patient  to  close  and  open  the  hand,  thus  forcing  the  blood  through 
the    veins   by    muscle    contraction. 

The  best  results  are  usually  secured  by  the  removal  of  300  to  500 
cubic  centimeters  of  blood. 

DIET 

There  are  few  general  principles  which  can  be  laid  down  as  a 
guide  in  regulating  the  diet  of  those  suffering  from  myocardial 
disease.  The  relation  of  protein  intoxication  to  the  degenerative 
changes  of  various  organs,  is  a  subject  pregnant  with  interesting 
possibilities,  but  as  yet  our  knowledge  is  but  a  step  advanced  be- 
yond the  sphere  of  pure  speculation.  If  our  therapeutics  are  to 
be  used  with  a  conviction  which  is  based  on  a  reasonable  logic, 
the  application  of  these  hypotheses  to  the  treatment  of  our  patients 
must  await  the  discovery  of  further  facts  which  may  link  together 
the    fragments   which  at  present  can  only  be  called  suggestive. 


Treatment 

The  beneficial  effects  of  the  administration  of  large  quantitie 
of  sugar  is  based  on  evidence  secured  by  perfusing  the  isolated 
heart  with  fluids  containing  sugars  of  varying  amounts'*'  and  is 
supported  by  a  considerable  amount  of  rather  unconvincing  clin- 
ical evidence. f  My  own  experience  with  this  procedure  has  been 
limited  and  thus  far  inconclusive. 

Regulation  of  the  diet  is  important,  but  should  be  directed  toward 
the  correction  of  conditions  frequently  very  remote:  from  the  hearl 
and  which  influence  the  myocardium  in  ways  indirect,  but  often 
efficacious. 

Among  such  conditions  the  patient's  weight  should  receive  con- 
sideration as  a  factor  of  first  moment.  Excessive  weight  is  a  very 
common  complication  of  chronic  heart  disease,  because,  as  a  rule, 
restriction  in  the  amount  of  food  has  not  paralleled  the  reduction 
in  bodily  activity.  The  requirements  of  the  body  at  rest  are  less 
than  twenty-five  calories  per  kilogram  of  body  weight.  Those  whose 
activities  call  for  great  physical  work  often  utilize  50  calories  per 
kilo.  When  a  patient's  mode  of  life  is  suddenly  changed  from 
one  of  severe  physical  exertion  to  one  of  comparative  inactivity, 
the  tendency  is  for  him  to  continue  taking  the  quantity  of  food 
which  habit  has  established.  As  a  result,  the  body  requirements 
are  more  than  supplied  and  the  surplus  is  stored  as  fat,  which 
soon  is  an  additional  burden  to  be  carried  by  a  heart  whose  reserve 
already  shows  too  narrow  a  margin.  It  follows  that  when  a 
physician  curtails  the  physical  activities  of  a  patient  with  an  in- 
sufficient heart,  the  diet  should  be  restricted  as  a  prophylactic  meas- 
ure. When  an  excessive  diet  has  already  produced  a  condition  of 
obesity,  the  overweight  must  be  gotten  rid  of  by  a  carefully  insti- 
tuted reduction  cure.  The  details  of  a  regime  suited  to  the  needs 
of  the  various  types  which  we  meet  need  not  detain  us,  but  we 
should  bear  in  mind  that  dependence  must  be  placed  almost  en- 
tirely on  the  restricted  caloric  value  of  the  ingested  food.  Exer- 
cises can  be  employed  to  only  a  very  limited  extent  and  drugs 
are  worse  than  valueless.  The  weight  should  be  reduced  very 
gradually.  I  believe  the  best  results  are  obtained  when  the  loss 
is  about  one  pound  a  week. 

*Locke  and  Rosenheim :  Zentralbl.  f .  Physiol.,  1905,  Xo.  20.  Dec.  30. 
fA.  Goulston :  Cane  Sugar  and  Heart  Disease,  London,  1914. 


256  Treatment 

The  antitheses  to  these  ohese  patients  are  not  infrequently  seen. 
They  are  below  average  weight  and  are  poorly  nourished.  Most 
often  they  are  young  persons  \\ln>  are  growing  rapidly.  Some- 
times they  have  had  repeated  attacks  of  rheumatic  fever.  The 
whole  musculature  is  below  par  and  the  myocardium  has  suffered 
along  with  the  other  muscles  of  the  body.  To  these  judiciously 
forced  feeding  is  of  great  value. 

Patients  suffering  from  chronic  nephritis  with  high  blood  pres- 
sure and  a  heart  laboring  beyond  its  capacity  are  best  treated 
dietetically  with  foods,  the  end  products  of  which  make  the  least 
demand  on  the  eliminative  capacity  of  the  kidney.  The  kind  of 
food  best  suited  to  the  individual  case  can  only  he  determined  by 
a  careful  study  of  the  functional  activities  of  the  kidney  in  each  case. 

Those  with  infectious  diseases  running  a  febrile  course  with  inter- 
current myocardial  involvement  should  be  fed  with  small  quantities 
of  nutritious  food  at  frequent  intervals.  The  management  of  the  diet 
does  not  differ  from  that  of  the  uncomplicated  disease,  except  that, 
as  a  rule,  it  is  well  to  keep  the  administration  of  fluids  within 
reasonable  bounds. 

In  general,  patients  with  well-marked  cardiac  insufficiency  do 
better  when  given  small  meals  at  frequent  intervals ;  five  or  six  feed- 
ings in  the  twenty-four  hours  are  usually  better  than  three  meals. 
The  majority  of  the  diet  should  consist  of  solid  food. 

Quite  as  important  as  the  proper  direction  of  the  kind  and  quan- 
tity of  the  food  is  the  regulation  of  the  water  balance.  The  rela- 
tion of  cedema,  ascites,  pleural  effusion,  etc.,  to  myocardial  insuffi- 
ciency is  intricate  and  a  full  discussion  would  lead  us  far  afield. 
The  volume  of  the  circulating  blood  undoubtedly  has  a  considerable 
influence,  not  only  on  the  amount  of  work  which  the  heart  is  called 
upon  to  perform,  but  also  must  be  reckoned  with  as  a  direct  factor 
in  producing  dilatation  and  hypertrophy.  The  most  notable  example 
of  this  condition  is  met  with  in  the  so-called  "beer  heart."  Here 
the  myocardial  changes  may  be  the  result  of  several  elements,  such 
as  the  alcohol  and  carbohydrate  content  of  the  beverage,  the  severe 
physical  exertion  to  which  most  of  these  patients  have  been  sub- 
jected and  the  increased  volume  of  the  blood  following  the  inges- 
tion of  enormous  quantities  of  fluid.  Practically  all  competent  ob- 
servers  are   agreed   that    the    latter    is    the    most    important    factor 


Treatment  257 

in  inducing  the  change  in  the  hear!  muscle.  The  aspiration  of  tin- 
pleura,  or  the  removal  of  ascitic  fluid,  will  often  relieve  the  -train 
on  a  laboring  heart  and  furnish  the  starting  point  for  the  recovery 
of  its  reserve  force.     The  disappearance  of  oedema  is  frequently 

the  forerunner,  rather  than  the  result,  of  improved  heart  action. 
With  this  end  in  view,  the  stimulation  of  kidney  activity  and  the 
reduction  of  the  sodium  chloride  intake  may  he  of  considerable 
indirect  benefit   to  the   heart. 

As  a  general  rule,  those  suffering  from  myocardial  insufficiency 
should  not  take  over  one  and  a  half  liters  of  fluid  a  day.  Many, 
particularly  those  having  oedema,  are  greatly  benefited  by  a  more 
restricted  fluid  intake.  We  are  not  as  yet  in  a  position  to  designate 
the  exact  types  which  will  respond  favorably  to  an  extreme  limi- 
tation of  fluid  ingestion,  but  not  infrequently  the  employment  of 
this  method  yields  brilliant  results.     The  diet  suggested  by  Karell* 

*Karrell  Diet.  For  the  first  five  to  seven  days,  milk  200  cc.  at  8  and  12  a.m., 
4  and  8  p.m.  No  other  food  or  fluid.  Eighth  day :  milk  as  above  and  at 
10  a.m.  one  soft-boiled  egg;  at  6  p.m.,  two  pieces  of  dry  toast.  Ninth  day: 
milk  as  above  and  at  10  a.m.  and  6  p.m.  one  soft-boiled  egg  and  two  pieces 
of  dry  toast.  Tenth,  eleventh  and  twelfth  days:  milk  as  above,  and  at  12  m. 
chopped  meat,  rice  boiled  in  milk  and  vegetables ;  6  p.m.,  one  soft-boiled 
egg.  (No  salt  is  used  throughout  the  course.  Salt-free  toast  and  butter 
used.  Small  amount  of  cracked  ice  allowed  with  diet.  All  meat  can  often 
be  advantageously  omitted.)  From  Dr.  Herbert  S.  Carter's  Diet  Lists, 
Saunders,   Phila.,   1914. 

is  one  of  the  most  satisfactory  means  of  securing  the  desired  fluid 
restriction.  During  such  a  course  the  patient  should  be  confined 
to  bed.  Not  infrequently  a  patient  who  has  shown  a  prompt  im- 
provement on  a  Karell  regime  may  be  benefited  by  later  using  such 
a  diet  one  day  each  week. 

BEVERAGES 

The  regular  use  of  alcohol  in  those  suffering  from  functional  or 
organic  disease  of  the  myocardium,  is  to  be  deprecated  on  theoret- 
ical grounds.  There  is  little  doubt  that  its  habitual  use  affects 
favorably  neither  the  heart  muscle  nor  its  controlling  nervous  mech- 
anism. And  yet  I  think  there  are  many  patients  accustomed  to  the 
use  of  malted  and  spirituous  liquors  by  years  of  habit  in  whom  the 
entire  withdrawal  of  all  alcoholic  beverages  is  a  distinct  detri- 
ment. To  young  adults,  all  alcoholic  drinks  should  be  forbidden : 
elderly  people  accustomed  to  its  use  often  do  better  if  allowed 


_'5S  Treatment 

moderate  quantities.  Light  wines,  good  whiskey  or  brandy  are  to 
be  preferred  to  malted  drinks  representing  an  equal  amount  of 
alcohol.  These  should  be  taken  at  meal-time  and  in  amounts  defi- 
nitely prescribed.  Tea  and  coffee  should  be  regulated  much  in  the 
same  way  as  alcohol,  tlu-\  are  not  to  be  indiscriminately  forbidden 
and  in  certain  instances  the  effect  dt"  the  contained  caffeine  is  of 
distinct  value. 

<  OLD  APPLICATIONS 

The  application  of  cold  to  the  precordium,  l>v  means  of  an  ice- 
bag  or  a  Leiter's  coil,  often  seems  to  be  of  advantage  in  rapid, 
overacting  hearts  and  in  tachycardias  of  sinus  origin.    The  rational 

explanation  of  such  a  procedure  present  difficulties.  We  know  that 
the  formation  of  stimulus-material  is  slowed  hv  a  direct  applica- 
tion of  cold  to  the  sinus  region,  but  it  is  hardly  conceivable  that 
a  precordial  icebag  will  produce  a  degree  of  cold  sufficient  to 
penetrate  to  such  a  depth. 

The  precordial  poultice  and  hot  fomentation  are  frequently  com- 
forting to  the  patient.  It  is  doubtful  whether  they  have  any  more 
profound  therapeutic  effect. 

BATHS 

In  a  certain  number  of  patients  suffering  from  myocardial  dis- 
ease, a  course  of  baths  seems  to  be  of  considerable  value.  Waters 
containing  carbon  dioxid  and  simple  brine  have  been  employed 
with  satisfactory  results.  The  reaction  of  the  individual  patient 
must  be  studied.  The  first  bath  should  be  a  weak  one,  just  below 
body  temperature  and  should  last  not  over  six  minutes.  It  the 
patient  is  comfortable,  if  there  is  no  increase  of  dyspnoea,  and  if 
the  pulse  .and  heart  action  are  improved,  the  baths  may  gradually 
be  made  stronger,  the  temperature  lowered  and  the  time  length- 
ened. The  method  is  almost  wholly  empirical  and  we  have  little 
knowledge  of  the  physiological  processes  through  which  the  bene- 
ficial results  are  obtained.  Nervous  reflexes,  following  cutaneous 
stimulation  and  altered  vaso-motor  tone,  are  probably  elements  of 
importance,  but  much  careful  observation  and  scientific  study  is 
necessary  before  we  can  offer  a  logical  explanation  of  the  modus 
operandi  and  a  more  accurate  outline  of  the  indications  for  and 
a'rahiNt  these  measures. 


Treatment  259 

SPA  TREATMENT 

The  value  of  spa  treatment,  I  believe,  has  been  greatly  over- 
estimated. The  benefits  derived  from  a  visit  to  a  well-organized 
resort  arc  due  mainly  to  the  ordered  regime  to  which  the  patienl 
is  subjected  under  the  watchful  care  of  a  skilful  physician,  the 
relaxation  from  the  cares  of  business  and  home,  the  change  of 
scene  and  opportunities  for  properly  regulated  pleasures.  The  spe- 
cific value  of  special  waters  and  complicated  apparatus  are  of  very 
minor  importance. 

The  miraculous  cures  which  are  often  claimed  in  the  name  of 
the  spa  may  be  equalled  in  the  experience  of  any  skilful  practitioner. 

Most  patients  are  much  more  readily  controlled  in  a  place  re- 
moved from  accustomed  ties  and  responsibility,  and  where  it  is 
the  fashion  to  follow  the  minute  directions  of  the  medical  adviser. 

The  conscientious  physician,  in  considering  the  probable  value  to 
be  derived  by  his  patient  from  spa  treatment,  must  take  into  account 
the  long  journey,  its  attendant  fatigue  and  expense.  He  must  see 
to  it  that  his  patient  is  placed  under  expert  medical  care  and  is 
not  allowed  to  drift  into  the  net  of  the  unbalanced  faddist  or  the 
unscrupulous  charlatan,  who  unfortunately  are  not  less  in  evidence 
at  the  most  famous  cures  than  elsewhere. 


CHAPTER  XVIII 

Treatment 
DRUGS 

In  the  present  discussion  of  drugs  in  the  treatment  of  abnormal- 
ities of  myocardial  function,  we  will  limit  ourselves  to  a  consid- 
eration of  a  very  small  number  and  will  examine  only  their  direct 
action  on  the  myocardial  tissues  or  their  indirect  action  through 
the  vagUS  and  accelerator  nerves. 

It  is  often  most  important  in  treating  myocardial  disorders  to 
correct  or  modify  the  condition  of  organs  other  than  the  heart. 
Thus  a  change  in  kidney  function  or  an  alteration  in  the  size  of 
the  peripheral  arteries  may  he  a  far  more  efficient  means  of  im- 
proving cardiac  function  than  anything  which  we  can  do  to  the 
heart  muscle  directly.  It  is  not,  however,  our  purpose  to  discuss 
drug  activity  from  this  standpoint.  We  will,  therefore,  confine 
our  attention  to  those  drugs  which  have  a  direct  action  on  the 
myocardium  and  will  omit  a  consideration  of  the  effect  of  the 
drugs  of  our  selected  list  upon  other  organs  of  the  body.  These 
aspects  are  presented  in  the  proportions  which  they  deserve  in 
the  standard  works  on  pharmacology  and  works  devoted  to  the 
broader  discussion  of  diseases  of  the  heart.  An  excellent  resume 
of  the  experimental  work  has  been  compiled  and  discussed  by  Win- 
terberg*  and  should  he  consulted  by  those  particularly  interested. 
The  graphic  methods  of  recording  circulatory  changes  have  greatly 
improved  the  detail  and  accuracy  of  our  clinical  observations.  By 
these  means  we  may  discover  minute  alterations  which  have  been 
hitherto  impossible  of  detection.  It  is  probable  that  the  next  few 
years  will  add  much  to  our  knowledge  of  the  usefulness  and  use- 
lessness  of  drugs. 

ADRENALIN 

The  extract  of  the  suprarenal  gland  finds  its  chief  effect  on  the 
wall  of   the  peripheral  blood  vessels.     There  is  considerable  evi- 

♦Handb.  d.  Path.,  Diagnostik,  u.  Tlicrap.  d.  Herz.  u.  Gefasskrankungen, 
Leipzig,  1914,  iii,  H.  2. 

260 


Treatment  261 

dence  that  it  also  has  an  influence  in  increasing  the  activities  of 
all  of  the  fundamental  properties  of  the  myocardial  cells,  notably 
heightening  the  irritability  and  the  contractility,  it  may  be  thai 
this  is  due  to  a  direct  action  on  the  muscle  cell  or,  indirectly, 
through  its  effect  on  the  sympathetic  nerve  for  which  this  drug 
seems  to  possess  a   selective  activity.* 

In  large  doses  and  under  special  conditions  (see  "ventricular 
fibrillation")  adrenalin  may  produce  extreme  myocardial  irritability 
and  many  types  of  arrhythmia. f 

On  account  of  its  influence  in  increasing  the  contractility  and  the 
tone  of  the  heart  muscle,  it  has  been  recommended  in  acute  dila- 
tation and  in  conditions  of  surgical  shock.  Until  our  knowledge 
is  more  complete,  I  believe  that  we  should  employ  adrenalin  with 
great  caution  in  conditions  of  acute  heart  failure,  recalling  that 
in  association  with  anaesthesias  of  light  degree^  it  has  a  tendency 
to  produce  great  irritability,  which  may  result  in  ventricular  fibril- 
lation and  a  fatal  outcome. 

There  is  considerable  experimental  evidence  which  indicates  that, 
while  adrenalin  acts  as  a  constrictor  on  most  of  the  peripheral 
arteries,  it  produces  a  widening§  of  the  lumen  of  the  coronaries. 

ALCOHOL 

The  effect  of  alcohol  on  myocardial  activity  is  probably  purely 
reflex  and  the  result  of  functional  changes  in  the  central  nervous 
system  and  modifications  of  vasomotor  control.  The  slowing  of 
the  heart,  following  the  administration  of  alcohol  in  febrile  affec- 
tions, is  probably  due  to  its  influence  in  diminishing  cerebral  ex- 
citement. Alcohol  has  no  effect  on  muscle  when  brought  to  it 
in  the  blood  stream,  but  when  applied  directly  to  the  muscle  it 
weakens  its  contractions  (Cushny). 

AMMONIA 

probably  has  no  direct  effect  on  the  myocardium.  Its  influence  in 
reducing  heart  rate  is  by  reflex  nervous  inhibition.  Its  effect  is 
quite  rapid  and  disappears  in  a  few  minutes. 

*Rothberger  and  YVinterberg :   Pfliiger's  Arch.,  191 1,  cxlii,  461. 
fKahn:  Arch.  f.  d.  ges.  Physiol.,  1909,  exxix,  379. 
tNobel  and  Rothberger:  Ztschr.  f.  d.  ges.  Exp.  Med.,  1914.  iii.  151. 
§Janeway  and  Park:  Jour.  Exp.  Med.,  1912,  xvi,  532,  541. 


_•<._•  Treatmi  n  r 

ATROPINE 
modifies  cardiac  activity  through  its  effect  on  the  vagus  nerve  con- 
trol.    It  probably  lias  no  direct  influence  on  the  myocardial  cells, 
although  given   in   toxic  quantities   to  experimental  animals   it   is 

said  to  depress  the  property  of  contractility  (Ringer).  The  first 
effect  of  atropine  is  to  stimulate  the  vagus  through  its  center  in 
the  medulla  and  thus  cause  a  slowing  oi  the  heart.  This  effect  is 
very  slight  and  quickly  passes  off.  It  is  succeeded  by  an  increase 
in  heart  rate  due  to  a  paralysis  of  the  inhibitory  terminations  oi 
the  vagus  nerves.  That  the  influence  is  due  to  its  action  on  the 
nerve  endings  is  indicated  by  the  fact  that  after  its  administration 
stimulation  of  the  vagi  has  no  effect  on  cardiac  activity,  whereas 
it"  the  action  were  central  stimulation  of  the  vagi  should  still  slow 
the    heart.      The   accelerators   are   not    affected    by    atropine. 

Children  show  very  little  cardiac  response  to  atropine.  The  reac- 
tion to  the  drug  gradually  increases  with  maturity  and  reaches  its 
maximum  in  those  about  thirty  years  of  age.  In  advanced  years 
the  reaction  is  less  marked  than  in  middle  life.  In  man  the  slow- 
ing of  the  heart  occurs  about  five  minutes  after  the  subcutaneous 
administration.  This  disappears  in  a  minute  or  two.  The  maxi- 
mum increase  in  heart  rate  appears  twenty  to  thirty  minutes  alter 
its  exhibition.  From  this  tune  the  rate  gradually  lessens  and  re- 
turns in  an  hour  or  two  to  the  rate  which  preceded  its  administration. 

Atropine  is  useful  in  correcting  a  heart  action  which  is  too  greatly 
slowed  by  an  overacting  vagus.  Thus,  in  a  heart  block  which  is 
due  to  a  hypertonic  vagus,  the  block  may  he  promptly  broken 
by  its  administration.  The  slowing  effect  of  morphine  may  he 
neutralized  by  atropine.  When  digitalis  has  been  given  to  excess, 
a  part  of  its  influence  may  he  promptly  opposed  by  a  hypodermic 
of  atropine.  Its  administration  is  a  useful  diagnostic  means  of 
distinguishing  the  vagal  influences  in  heart  block  and  cases  of  sus- 
pected hypervagotonicity  from  those  in  which  the  defect  is  intrin- 
sically in  the  muscle  cell.  If  the  disordered  myocardial  function 
is  due  to  an  excessive  activity  of  the  vagus,  the  atropine  will  speed- 
ily remove  this  influence. 

In  an  adult  with  a  heart  rate  under  60,  1.3  milligrams  (  i/5° 
grain  1  may  he  given  subcutaneously  and  may  he  repeated  when 
the  effect  has  disappeared.     Unfortunately,  the  drug  is  not   well 


Treatment  263 

suited  for  prolonged  therapeutic  effects,  for  if  the  dosage  is  con- 
tinued at  a  level  to  maintain  the  vagus  paralysis  other  symptoms, 
such  as  dryness  of  the  pharynx,  dilatation  of  the  pupil,  etc.,  make 
the  patient  very  uncomfortable. 

CAFFEINE 

and  the  closely  related  substances,  theobromine  and  theophyllin, 
exert  an  influence  on  both  the  extracardial  nerves  and  on  the  muscle 
cells  of  the  heart.  In  experimental  animals  caffeine  may  slow  the 
heart  by  central  stimulation  of  the  vagus  and  depression  of  the 
accelerators  (Fredericq).  \n  man  such  an  effect  is  very  incon- 
stant. Small  doses  in  animals  usually  accelerate  the  heart  by  in- 
creasing the  irritability  of  the  sinus  node  (Cushny  and  Naten*). 
This  effect  is  independent  of  any  action  on  the  regulatory  mechan- 
ism of  the  heart,  since  it  is  seen  when  the  accelerators  are  cut 
and  when  the  vagus  is  paralyzed  by  atropine.  In  dogs  large  doses 
produce  auriculo-ventricular  dissociation  (depression  of  conduc- 
tion). In  animals  in  which  an  artificial  heart  block  has  been  pro- 
duced by  a  destruction  of  the  bundle  of  His,  caffeine  augments 
the  irritability  of  the  ventricle  so  that  the  ideo-ventricular  rate  is 
increased  and  many  extrasystoles  appear.f  The  evidence  as  to  the 
effect  of  caffeine  on  contractility  is  somewhat  conflicting,  but  in- 
clines toward  the  view  that  in  moderate  doses  it  improves  the 
working   efficiency    of   the   heart. 

In  a  few  patients  to  whom  I  have  administered  theocin  as  a 
diuretic,  there  have  appeared  immediately  thereafter  large  num- 
bers of  extrasystoles  and  in  one  case  a  paroxysm  of  tachycardia, 
which,  as  far  as  could  be  determined,  was  unique  for  this  indi- 
vidual. These  observations  have  led  me  to  be  cautious  in  the  use 
of  caffeine  and  closely  related  drugs  in  myocardial  conditions  show- 
ing a  high  degree  of  irritability.  It  suggests  that  the  excessive 
use  of  tea  and  coffee  in  susceptible  individuals  may  be  the  cause  of 
extrasystoles. 

CAMPHOR 

is  one  of  our  drugs  which  has  long  enjoyed  a  reputation  as  a 
direct  stimulant  to  cardiac  muscle.  We  have  at  present  no  con- 
clusive evidence  that  it  favorably  affects  the  heart  muscle.     Its  use 

*Arch.  Internal:,  de  Pharmodyn  et  de  Therapie,  1901,  ix,  169. 
fEgmond :  Pniiger's  Arch.,  1913,  cliii,  39. 


264  Treatment 

has  been  advocated  in  auricular  fibrillation,  but  recent  reports  make 
it   appear  that   it   is  of  doubtful   value  in  this  condition. 

CHLOROFORM 

acts  on  the  heart  indirectly  by  stimulating  the  vagus  center,  thus 
slowing  the  heart,  and  also  has  a  direct  influence  on  the  muscle 
cells  of  the  heart.  Chloroform  depresses  conductivity  to  such  an 
extent  that  at  times  an  auriculo-vcntricular  block  is  established.  It 
may  greatly  increase  the  irritability  of  the  ventricular  wall  so  that 
mam  extrasvslolcs  appear  which  may  pass  into  a  ventricular  tachy- 
cardia and  thence  to  ventricular  fibrillation  which  is  uniformly 
fatal.  The  observations  of  Levy*  seem  to  indicate  that  the  most 
detrimental  effects  to  the  myocardium  are  wont  to  occur  during 
light  aiuesthesia,  so  that  arrhythmias  are  most  common  when  the 
patient  is  in  the  early  stages  of  anaesthesia  or  is  beginning  to 
recover  from  its  effects.  The  dangers  of  the  use  of  adrenalin,  in 
conjunction  with  chloroform,  have  already  been  noted  (see  "ven- 
tricular  fibrillation"   and   "adrenalin"). 

DIGITALIS 

Digitalis  obtained  from  the  purple  foxglove  is  the  most  impor- 
tant member  of  a  group  of  drugs  which  have  a  similar  action  on 
the  heart.  In  this  series  are  included  strophanthus,  squills,  helle- 
bore, convallaria,  apocynutn  and  several  others  less  well  known. 
Of  this  group  of  drugs  digitalis  has  received  by  far  the  greater 
study  and,  since  all  the  members  of  this  series  affect  the  myocardium 
in  a  similar  manner,f  our  discussion  will  be  in  the  main  limited 
to  digitalis  and  the  alkaloids  which  are  derived  from  it.  The 
glucosides  obtained  from  digitalis  include  digitoxin,  digitophyllin, 
digitalin,  digitalein  and  digitonin.  All  of  these  glucosides  are  pres- 
ent in  the  infusion;  digitonin,  being  insoluble  in  alcohol,  is  absent 
from  the  tincture. 

Pharmacological  studies  indicate  that  digitalis  acts  in  a  twofold 
manner  on  the  functional  activities  of  the  heart.  It  has  a  direct 
effect  on  the  muscle  cells  and  an  indirect  influence  through  the 
vagus  nerves.  The  influence  on  the  fundamental  properties  of 
the  muscle  cells  has  been   analyzed  to   some  degree.      Tunc:  this 

♦Heart:   1913,  iv,  319. 

tCushny:  Jour.  Exp.  Med.,  1897,  ii,  233. 


265 


Figure  203 

Digitalis    effect.      Delayed    conduction.      a-c    intervals  —  0.4    second. 


Figure  204 

Digitalis   effect.      2  to    1   block.      Auricular   rate   80.      Ventricular   rate  40. 


Jugular 


Brachial 


Jugular 


Brachial 


0.2  second 


Jugular 


Brachial 


0.2  second 


Figure  205 

Digitalis  effect.      Coupled   rhythm   in  a  case   of  auricular  fibrillation. 


266  Treatment 

property  is  distinctly  modified  by  digitalis,  its  direct  action  on  the 
muscle  is  to  increase  its  tone  and  to  render  relaxation  less  com- 
plete, the  heart  becomes  smaller  in  s]  stole  and  dues  not  dilate 
.so  fully  in  diastole.  Hand  in  hand  with  this  direct  action  on  the 
muscle,  digitalis  exerts  a  stimulating  effect  on  the  vagi,  through 
this  influence  the  heart  is  slowed  and  the  tendency  to  diastolic  re- 
laxation is  increased.  Hence,  the  effect  of  digitalis  on  cardiac 
tone  is  the  resultant  of  these  two  opposed  factors  and  the  tonicity 
will  he  increased  or  diminished  according  as  the  direct  muscle  effect 
or  the  indirect  vagus  effect  is  predominant.  In  a  like  manner 
the  efficiency  of  the  heart  to  empty  itself  will  depend  on  the  rela- 
tive degree  to  which  each  of  these  factors  comes  into  play.  Con- 
ductivity is  depressed  so  that  one  often  sees  in  the  experimental 
animal  a  complete  auriculo-ventricular  block.  The  depression  of 
conductivity  is  due  in  part  to  vagus  influences,  since  the  block  can 
at  times  be  removed  by  cutting  the  vagi.  However,  there  is  some 
evidence  which  suggests  that  the  dissociation  is  also  due  to  a 
direct  action  of  digitalis  on  the  cells  of  the  myocardium.  The 
irritability  of  the  heart  muscle  is  increased  by  digitalis.  Thus, 
in  the  isolated  heart  which  has  ceased  to  heat,  the  addition  of 
digitalis  to  the  perfusion  fluid  may  induce  rhythmic  contractions. 
All  these  modifications  of  the  fundamental  properties  of  the  heart 
muscle  which  have  heen  ohserved  in  the  experimental  animal  may 
be  seen  in  man.  We  have  as  yet  no  accurate  means  of  meas- 
uring the  tonicity  of  the  heart  in  the  human  subject,  hut  most 
clinicians  believe  that  it  is  increased  by  the  administration  of  drugs 
of  the  digitalis  group.  A  depression  of  conduction,  even  to  the 
degree  of  complete  auriculo-ventricular  dissociation  and  increased 
irritability  (as  evidenced  by  the  production  of  extrasystoles),  are 
common  sequela:  of  the  exhibition  of  digitalis  in  the  clinic. 

While  the  experimental  study  of  digitalis  has  afforded  us  much 
valuable  information  in  regard  to  the  nature  of  its  activity,  it  should 
be  remembered  that  such  investigations  must  of  necessity  he  car- 
ried out  on  hearts  with  a  myocardium  approaching  the  normal  or 
the  damage  which  has  been  artificially  produced  is  an  acute  change 
which  is  probably  quite  different  from  the  myocardial  changes  which 
are  commonly  seen  in  the  clinic  and  checked  up  at  the  post-mortem 
examination. 


-'7 


I     •        : 


PR         VR 


*f*tf**{**f*f*"fHi^^ 


S  5 


Figure  2nt> 
February  24,  1916.     Before  digitalis. 


PR         -pn 


^f*"0f*^f**"*P~*f**f**0fm"( 


Figure  207 

March    9,    1916.      Sinus   slowing. 


LTZHF 


rr  1    r 


P  R 


R     P  PR  -P     *a 


Figure  208 

March    13,    1916.      Complete   block. 


Figure  209 

March  15,  1916.  Complete  block  and  coupled  rhythm.  Every  other  ventricular  beat 
is  an  extrasystole. 

All  these  records  are  from  the  same  patient  and  show  the  progressive  effect  of  con- 
siderable doses  of  digitalis  in  a  myocardium  susceptible  to  its  influence.  All  of  these 
records  were  taken  by  lead  III. 


268  Treatment 

It  is,  therefore,  most  fortunate  that  the  polygram  and  electro- 
cardiogram have  come  to  <>ur  aid  in  the  study  of  the  effects  o\ 

this  and  other  drugs  in  man  under  the  conditions  which  arc  seen 
in   health   and   disease  and    which   it    is   impossible   to   reproduce   in 

the  experimental  animal. 

The  alterations  in  the  rhythm  of  the  heart  under  the  influence  ol 
digitalis  are:  (i)  a  slowing  (due  to  a  depression  of  stimulus  for- 
mation at  the  sinus  node  induced  by  vagal  influences)  ;  (2)  a  slow- 
ing and  development  of  arrhythmia,  with  modification  of  the  prop- 
erty of  conduction  (due  to  change  in  the  A-V  junctional  tissues 
through  a  direct  effect  on  the  myocardium  and  an  indirect  effect 
through  the  vagus),  and  (3)  an  increased  irritability  causing  new 
forms  of  irregularity  to  appear  (extrasystoles,  fibrillation,  etc.). 
Some  of  these  changes  may  be  detected  by  the  ordinary  methods 
of  physical  examination.  The  change  in  rate  of  sinus  origin  is 
usually  only  of  moderate  degree;  when  due  to  alteration  in  con- 
duction, the  slowing  may  he  much  more  marked,  so  that,  with 
complete  hlock,  the  ventricular  rate  may  he  reduced  to  30  a  min- 
ute. These  conduction  changes  may  sometimes  he  verified  by  ob- 
serving the  rate  of  the  jugular  pulsations  in  the  neck  and  comparing 
them  with  the  apex  impulse  (see  "conduction  defects,"  Chapter 
VI).  The  increase  in  irritability  is  identified  by  watching  for  the 
development  of  complete  irregularity  (see  "auricular  fibrillation," 
Chapter  XI)  or  of  extrasystoles  (see  Chapter  VII),  notably  the 
so-called  "coupled  rhythm,"  in  which  two  beats  are  followed  by  a 
pause:  the  second  of  these  beats  is  an  extrasystole  and  the  pause 
is  the  ordinary  "compensatory  pause"  which  is  associated  with 
extrasystoles.  At  first  this  digitalis  effect  may  he  observed  as  oc- 
casionally occurring  extrasystoles,  later  every  other  heart  contrac- 
tion is  an  extrasystole  with  a  compensatory  pause  and  this  is  man- 
ifested as  the  "coupled  rhythm." 

The  polygram  helps  us  in  detecting  these  digitalis  effects  and 
is  a  much  more  accurate  indicator  of  the  changes  in  heart  rhythm 
than  inspection,  palpation  and  percussion. 

Records  from  three  cases  under  the  influence  of  digitalis  may 
be  seen  in  Figures  203,  204  and  205.  In  Figure  1  the  a-c  inter- 
val is  greatly  prolonged  and  measures  0.4  second.  In  the  case 
whose   curve    is    shown    in    Figure   204   the   brachial    pulse    rate   is 


Digitalis 


269 


Figure  210 

Coupled  rhythm.      Digitalis  effect  in  a  case  of  auricular   fibrillation. 


Figure  211 

Coupled   rhythm.      Digitalis  effect.      Every    other   ventricular    beat   is   an    e.xtrasvstole. 
Case  of  auricular  fibrillation. 


270  Treatment 

perfectly  rhythmic  and  only  40  a  minute;  the  auricular  rate  is  80 
and  the  slow  ventricular  rate  is  due  to  a  2  to  1  block.  The 
patient  whose  tracing  is  presented  in  Figure  205  was  a  case  of 
auricular  fibrillation  which  showed  the  toxic  effects  of  digitalis 
by  the  development  of  the  coupled  rhythm;  the  brachial  shows  a 
rate  dt  67  per  minute,  hut  examination  of  the  jugular  curve  shows 
that  the  ventricle  was  beating  at  a  rate  of  ij.|  per  minute,  hut 
only  every  other  one  of  these  heats  makes  an  impression  on  the 
brachial  curve.  'The  second  heat  of  the  couple  is  a  ventricular  ex- 
trasystole  and  is  followed  by  a  compensatory  pause.  A  rhythm  of 
this  character  and  of  such  a  rate  indicates  a  high  grade  of  irri- 
tability of  the  ventricular  muscle  and  is  a  warning  that  digitalis 
must    he    immediately    discontinued. 

The  electrocardiograms  bring  out  these  changes  even  more 
clearly.  Figures  206,  207,  208  and  20<;  are  all  taken  from  the  same 
patient  at  intervals  of  a  few  days  during  the  administration  of 
digitalis.  Figure  206  presents  the  rapid  rate  (  145)  with  a  normal 
P-R  interval  hefore  digitalis  was  commenced.  (All  these  figures 
record  lead  111,  in  which  in  this  case  the  .V  wave  was  abnormally 
deep,  suggesting  left  ventricular  preponderance;  see  Chapter  XVI.) 
In  Figure  207  is  seen  a  slowing  of  the  whole  heart  1  sinus  effect) 
and  prolonged  P-R  interval  (.-/-/'  conduction  delay).  Figure  208 
shows  still  greater  sinus  slowing  and  a  partial  block.  Figure  209 
portrays  an  even  less  rapid  sinus  activity,  complete  block  and  the 
"coupled  rhythm,"  in  which  the  second  heat  of  each  pair  is  a 
ventricular  extrasystole,  indicating  a  high  degree  of  myocardial 
irritability. 

Records  of  two  cases  of  auricular  fibrillation,  with  different  grades 
of  ventricular  irritability,  are  presented  in  Figures  210  and  211. 
It  is  quite  evident  that  the  irritability  of  the  heart  recorded  in 
Figure  211  is  very  extreme,  much  more  than  that  shown  in  either 
Figures  209  or  210.  There  is  another  very  interesting  change  in 
the  electrocardiographic  records  under  the  administration  of  digi- 
talis which  has  been  recently  described  by  Cohn,  Fraser  and  Jamie- 
son.*  This  consists  in  a  change  in  the  contour  of  the  T  wave.  A 
T  wave  which  is  positive  in  direction  before  the  use  of  digitalis 
becomes   smaller,   diphasic  or   even   directed   downward   when   the 

*Jour.  Exp.  Mod.,   1915,  xxi,  593. 


_7-  l'ki' \TMKNT 

heart  becomes  digitalized.  This  is  well  shown  by  comparing  Fig- 
ures 212,  213  and  J14,  the  three  leads  taken  before  and  Figures 
215,  216  and  -17  secured  after  the  administration  of  digitalis.  This 
sign  is  a  valuable  guide  in  determining  whether  the  heart  muscle 
is  being  affected  by  the  digitalis.  The  discoverers  found  it  as  the 
earliest  evidence  of  digitalization  in  34  out  of  36  cases.  They  also 
call  attention  to  the  fact  that  influences  other  than  digitalis  may, 
on  rare  occasions,  produce  a  similar  modification  of  the  size  and 
direction  of  the  T  wave. 

There  is  considerable  clinical  evidence  that  digitalis  acts  both 
on  the  muscle  cells  of  the  heart  directly  and  indirectly  through  the 
vagi.  The  changes  which  occur  in  the  T  wave  suggest  this.* 
If  the  heart  is  brought  thoroughly  under  the  influence  of  digitalis, 
and  tlie  vagal  influences  are  removed  by  administering  atropine 
which  paralyzes  the  terminals  of  the  vagus  in  the  myocardium,  cer- 
tain digitalis  effects  will  still  persist.!  Digitalis  has  a  greater  in- 
fluence on  the  damaged  than  on  the  normal  heart  muscle.  This 
is  particularly  true  of  hearts  which  have  been  injured  as  the  re- 
sult of  rheumatic  fever  and  those  which  show  conduction  defects. 
Digitalis  is  particularly  indicated  in  the  dilated  heart  with  a  re- 
duced muscle  tone  and  in  cases  of  tachycardia,  where  the  rapid 
ventricular  rate  is  due  to  impulses  arising  in  abnormal  foci  in  the 
auricles  which  are  showered  upon  the  A-V  junctional  tissues 
(auricular  fibrillation  and  auricular  flutter)  ;  here  it  is  given  with 
the  purpose  of  blocking,  partially  or  completely,  the  stimuli  from 
the  upper  chambers. 

Digitalis  is  usually  contraindicated  in  those  showing  frequent  ex- 
trasystoles,  unless  it  can  be  shown  by  careful  observation  that  it 
does  not  increase  the  myocardial  irritability. 

It  is  rarely  of  value  in  tachycardias  of  sinus  origin  such  as  are 
seen  in  certain  forms  of  auricular  paroxysmal  tachycardia,  Graves' 
disease  and  in  the  acute  infections.  In  hearts  showing  a  partial 
block  the  abnormality  is  usually  increased  by  digitalis  administra- 
tion.    It  is  not  contraindicated  by  hypertension. 

When  a  digitalis  action  is  desired,  it  should  be  given  until  some 
physiological  effect  becomes  apparent,  but  in   pushing  the  dosage 

*Cohn:  Jour.  Amer.  Med.  Assn.,  1915,  lxv,  1527. 

fCushny,  Morris  and  Silberberg:  Heart,  1912-13,  iv,  33;  Talley:  Amer. 
Jour.  Med.  Sc,  1912,  cxliv,  514. 


Treatment  273 

the  possible  dangers  should  never  be  forgotten.  Evidences  of  heart 
block  and  excessive  irritability  must  be  watched  for  and  their  de- 
velopment are  the  signs  which  should  at  once  put  us  on  guard. 

The  most  important  elements  in  selecting  particular  preparations 
of  digitalis  for  administration  are:  (i)  a  high  degree  of  physio- 
logical activity;  (2)  uniformity  of  physiological  activity,  and  (3) 
familiarity  on  the  part  of  the  physician  with  the  physiological  ac- 
tivity. One  and  two  can  only  he  secured  hy  obtaining  the  drug 
from  reliable  manufacturers  who  carefully  select  their  digitalis 
leaves,  employ  a  uniform  method  of  extracting  the  active  prin- 
ciples and  standardize  their  product  by  physiological  tests.  The 
third  element  is  secured  by  confining  one's  attention  to  the  study 
of  a  small  number  of  preparations  and  using  these  to  the  exclu- 
sion of  all  others.  In  my  own  practice  a  potent  infusion,  a  stand- 
ardized tincture,  tablets  of  digipuratum,  ampoules  of  digipuratum 
and  crystalline  strophanthine  are  the  preparations  which  I  have 
found  satisfactory  and  which  meet  my  needs.  No  rules  for  the 
amount  of  the  drug  which  should  be  given  can  be  laid  down.  Each 
case,  in  this  respect,  is  a  law  unto  itself,  and  the  amount  can  be 
gauged  only  by  studying  the  physiological  effect  in  the  individual. 
The  maximal  doses  which  may  be  used  are:  of  an  active  infusion 
(freshly  prepared)  30  cc.  (1  ounce)  in  24  hours;  of  a  good  tinc- 
ture 4  cc.  (1  fluiddram)  in  24  hours;  digipuratum  by  mouth  0.4 
gram  (6  grains)  in  24  hours,  intramuscularly  0.1  gram  (1^2 
grains)  three  times  a  day;  crystalline  strophanthine  intravenously 
Yz  milligram  dissolved  in  8,000  parts  of  normal  saline,  not  more 
often  than  once  in  24  hours. 

Unless  there  is  special  urgency,  digitalis  should  be  given  by 
mouth,  as  all  of  the  active  preparations  are  very  irritating  to  the 
tissues  when  administered  subcutaneously.  Hatcher  and  Eggles- 
ton*  have  shown  that  the  nausea  and  vomiting  which  are  produced 
by  digitalis  is  due  to  their  action  on  the  central  nervous  system, 
rather  than  a  local  irritant  effect  on  the  stomach,  hence  the  intra- 
muscular or  intravenous  administration  causes  these  symptoms  as 
readily  as  when  the  drug  is  given  by  mouth.  The  toxic  dose  of 
strophanthin  given  intravenously  is  not  far  removed  from  the 
therapeutic  dose,  hence  it  should  never  be  given  to  a  patient  who 

*Jour.  Pharm.  and  Exp.  Therap.,  1912,  iv,  97. 


274  Treatment 

has  been  recently  taking  any  drugs  of  the  digitalis  series,  and  is 
indicated  only  in  extreme  emergencies. 

The  experimental  work  of  Voegtlin  and  Macht,*  who  found  that 
digitonin  relaxes,  while  other  alkaloids  of  digitalis  constrict,  the 
coronar\-  arteries,  suggests  that  in  coronary  spasm  the  infusion 
which  contains  digitonin  should  he  a  more  useful  preparation  than 
the  alcoholic  extracts  which  contain  no  digitonin. 

Digitalis  is  a  drug  of  great  power,  our  most  potent  agent  in 
correcting  certain  defects  of  myocardial  function,  hut  its  promiscu- 
ous use  is  not  without  danger  and  may  be  the  direct  cause  of  myo- 
cardial damage.  In  some  cases  it  is  absolutely  contraindicated,  in 
others  it  should  be  used  boldly  and  with  confidence.  In  those  in 
which  its  use  is  of  doubtful  value,  it  should  be  administered  with 
extreme  caution. 

OPIUM 

and  its  alkaloids  are  not  contraindicated  by  myocardial  lesions  po- 
se, although  the  associated  derangement  of  other  organs  (e.g.,  the 
kidneys)  may  make  their  use  inadvisable.  Their  effect  on  the 
heart  is  probably  entirely  due  to  a  stimulation  of  the  vagus  center 
in  the  medulla.  In  animals  large  doses  of  morphine  slow  the 
heart  rate.  This  effect  may  be  prevented  or  abolished  by  cutting 
the  vagi  or  by  the  administration  of  atropine.  It  may  produce||  a 
sino-auricular  or  an  auriculo-ventricular  block  and  other  forms  of 
arrhythmia,  notably  sinus  irregularities.  It  is  believed  that  these 
changes  are  entirely  due  to  vagus  influencesf  (some  hold  that  the 
accelerators  are  also  depressed)  and  that  morphine  has  no  direct 
action  on  the  muscle  of  the  heart.  In  man  therapeutic  doses  of 
morphine  produce  bradycardia  in  susceptible  individuals. 

Morphine  is  of  considerable  value  in  some  cardiac  emergencies, 
such  as  the  paroxysmal  tachycardias  and  other  rapid  hearts  asso- 
ciated with  conditions  of  great  excitement  and  restlessness. 

According  to  Macht, i  the  various  alkaloids  of  opium  differ  in 
their  effect  on  the  coronary  arteries.  Thebain,  heroin  and  codeine 
have  little  influence  on  controlling  the  lumen  of  these  blood  ves- 

*Jour.   Pharm.  and   Exp.  Therap.,    1913-14,  v,  76. 
||Eyster  and  Meek:  Heart,  1912,  iv,  59. 
tCohn  :  Jour.  Exp.  Med.,   1913,  xviii,  715. 
tMaclit:  Jour.  Amer.  Med.  Assn.,  1915,  Ixiv,  1489. 


Treatmeni  275 

sels ;  papavcrin  causes  a  marked  relaxation  and,  therefore,  should 
be  useful  in  anginal  pains  due  to  coronary  spasm. 

THE  NITRITES 
in  man  cause  a  considerable  acceleration  of  the  pulse  through 
reflex  influences  acting  on  tbe  vagus  center.  This  activity  may 
be  so  marked  that  apparently  the  vagus  is  completely  inhibited 
so  that  the  condition  simulates  full  doses  of  atropine.  It  seems 
pretty  well  established,  however,  that  these  influences  are  exerted 
on  the  medullary  center  and  not,  as  is  the  case  with  atropine,  on 
the  terminations  of  the  vagus  nerve.  Experiments  on  animals  and 
clinical  observations  have  failed  in  affording  evidence  that  the  ni- 
trites have  any  direct  action  on  the  heart  muscle.  Hence,  when  it 
is  indicated  by  reason  of  its  other  activities,  it  is  not  contraindi- 
cated  on  account  of  any  action  detrimental  to  the  myocardium. 

Extracts  of  the  posterior  lobe  and  the  pars  intermedia  of 
the  pituitary  gland  have  a  considerable  effect  on  the  peripheral 
arteries  and,  aside  from  this,  probably  a  direct  action  on  the  heart 
muscle.  According  to  Wiggers,*  they  slow  the  heart,  decrease  its 
amplitude  and  increase  its  muscle  tone. 

STRYCHNINE 

has  no  direct  action  on  the  cells  of  the  myocardium.     Its  effect  on 
the  heart  is  an  indirect  one  only  and,  therefore,  it  cannot  fairly 
be  classed  as  a  drug  useful  in  correcting  intrinsic  heart  defects. 
*Amer.  Jour.  Med.  Sc,  1911,  cxli,  502. 


CHAPTER  XIX 

Treatment 
INDICATIONS    AFFORDED    BY    THE    DIFFERENT    TYPES   OF    RHYTHM 

It  is  well  to  emphasize  at  the  outset  thai  the  individual  arrhyth- 
mias do  not  constitute  distinct  entities.    They  are  merely  symptoms 

of  abnormal  myocardial  activity.  At  times  an  arrhythmia  is  the 
only  means  through  which  we  may  detect  functional  disorders  of 
the  heart,  at  others  it  is  merely  one  of  a  large  group  of  signs  which 
demonstrate  the  defective  character  of  the  method  in  which  the 
heart  is  performing  its  work.  Their  special  value  is  found  in 
the  fact  that  they  often  reveal  the  particular  fundamental  prop- 
erties of  the  muscle  cells  which  are  at  fault,  and  thus  suggest  a 
new  point  to  be  attacked  by  therapeutic  measures.  The  treatment 
of  symptoms  is  often  of  very  great  value  not  only  because  a 
symptom  in  itself  may  at  times  actually  endanger  life,  but  also 
because  its  removal  may  be  the  starting  point  which  leads  to  the 
correction  of  the  more  fundamental  defect.  The  relief  of  pain 
during  an  acute  infection  may  afford  the  rest  which  the  body 
needs  to  reorganize  its  forces  to  combat  successfully  the  toxins 
which  are  threatening  its  life.  A  bradycardia  or  a  tachycardia  may, 
through  its  intensity  or  frequent  repetition,  jeopardize  life  quite 
aside  from  the  intrinsic  influence  which  the  underlying  lesion  may 
have  on  the  circulation. 

For  these  reasons  I  think  we  are  fully  justified  in  considering 
the  arrhythmias  in  separate  groups,  both  for  the  sake  of  such  clues 
as  may  thus  be  afforded  for  their  correction,  as  well  as  for  the 
light  which  such  a  classification  may  throw  on  the  conditions  more 
fundamentally  at  fault. 

It  is  needless  to  say  that  there  is  no  drug  or  therapeutic  measure 
which  is  a  specific  in  correcting  all  irregularities  of  the  heart.  One 
form  of  treatment  may  be  most  beneficial  in  one  type  of  arrhyth- 
mia and  absolutely  contraindicated  in  another  type.  This  becomes 
perfectly  apparent  when  we  consider  that  to  produce  the  different 
irregularities,  modifications  of  different  fundamental  properties  of 
the  myocardial  cells  are  necessary.     A  measure  which  may  satis- 

276 


Treatment  277 

factorily  control  one  form  of  arrhythmia  may  increase  or  even 
bring  into  being  another  type  of  irregularity. 

HEART  BLOCK 

is  the  type  of  abnormality  which  indicates  that  there  is  an  inter- 
ference with  the  conduction  of  stimuli  from  one  portion  of  the 
myocardium  to  another.     Fundamentally,  the  objeel   for  treatmenl 

is  to  restore  to  the  normal  the  functional  capacity  for  conduction. 

The  methods  to  be  selected  in  the  treatmenl  of  heart  block  depend 
upon  the  etiology,  the  degree  of  the  impairment  of  the  property 
of  conduction  and  the   functional  efficiency  of  the  heart. 

One  most  often  sees  a  condition  of  delayed  conduction,  or  of 
partial  block,  in  the  course  of  one  of  the  acute  infections,  notably 
in  cases  of  rheumatic  fever.  Usually  this  functional  disturbance 
is  transitory  and  passes  off  with  the  elimination  of  the  toxins  of 
the  acute  process.  The  treatment  is  entirely  directed  toward  the 
general  disease,  antitoxin  in  diphtheria,  salicylates  in  rheumatism, 
etc.,  free  elimination  in  all.  No  treatment  is  especially  indicated 
by  the  myocardial  defect,  which  doubtless  is  frequently  a  chemical 
alteration  rather  than  any  histological  change.  If  the  conduction 
abnormality  persists  after  the  acute  stages  of  the  disease  and  into 
the  period  of  convalescence,  the  patient  should  limit  his  activities 
for  a  considerable  time,  in  the  hope  that  the  heart,  not  unduly  taxed, 
may  recover  its  normal  function.  If,  after  a  reasonable  period,  the 
defect  appears  to  have  become  permanent,  the  patient  may  graduallv 
resume  his  usual  activities,  but  under  the  careful  observation  of 
his  physician,  in  order  that  an  increased  degree  of  block  or  anv 
cardiac  insufficiency  may  be  detected  at  once  and  be  corrected  by 
appropriate  measures. 

The  change  from  partial  to  complete  block  is,  of  course,  always 
abrupt,  but  there  are  certain  cases  which  show  what  we  may  desig- 
nate as  a  transition  period;  that  is  to  say,  a  very  moderate  block 
may  become  a  partial  block  of  marked  degree  and  then  return 
to  a  block  of  less  severe  type,  or  a  partial  block  may  become 
complete  and  in  the  course  of  a  few  hours  the  rhythm  may  revert 
to  the  partial  type.  As  has  been  pointed  out,  it  is  during  this 
period  that  the  patient  is  most  likely  to  develop  syncopal  attacks 
and  hence  is   in  a  condition  pregnant  with  considerable  danger. 


-'7N  Treatmen  r 

During  this  period,  resf  in  bed  should  be  insisted  upon;  this  not 
only  minimizes  the  possible  dangers  from  the  attacks  of  unconsciousr 
ness,  but  also  reduces  the  demands  on  the  heart  to  the  lowest  degree, 
thus  possibly  preventing  a  more  advanced  type  of  block  and  avoid- 
ing the  attacks  of  syncope.  It  is  in  this  period  that  atropine  may 
often  be  used  to  advantage.  (  u"  tins  mine  will  be  said  in  a  later 
paragraph.     Digitalis  is  contraindicated. 

Those  in  whom  complete  dissociation  is  thoroughly  established 
usually  can  resume  a  moderate  degree  of  activity,  unless  this  is 

found  to  reduce  the  ventricular  rate  or  to  induce  attacks  of  Syn- 
cope. Those  who  are  subject  to  attacks  of  unconsciousness  must 
limit  their  activities,  hut  are  not,  as  a  rule,  confined  to  bed.  They 
should  he  warned  of  the  dangers  which  the  fits  entail  and  should 
never  go  about  unattended.  Some  of  these  syncopal  attacks  seem 
to  have  a  definite  exciting  cause,  such  as  the  stress  of  over-exertion 
or  a  reflex  induced  by  gastrointestinal  disturbances.  Such  causes 
should  be  thoroughly  searched  for,  and  the  necessary  measures  for 
their  avoidance  instituted.  There  are  reports  in  the  literature  which 
seem  to  indicate  that  some  attacks  of  unconsciousness  can  be 
warded  off  or  aborted  by  the  use  of  atropine.  We  have  no  other 
means  of  relieving  the  syncopal  attacks  and  I  see  no  reason  why 
atropine  should  not  be  tried. 

With  ivw  exceptions,  complete  block,  when  once  established, 
continues  until  the  patient  dies.  From  our  knowledge  of  the  pathol- 
ogy, we  can  rarely  expect  to  restore  the  tissues  to  a  normal  capacity 
for  conduction  ;  however,  the  possibility  of  a  syphilitic  lesion  and  its 
removal  should  never  be  overlooked.  In  the  presence  o!  the  his- 
tory of  infection  and  a  positive  W'assermann  reaction,  a  vigorous 
course  of  antisyphilitic  treatment  is  always  indicated  and  even 
those  in  whom  the  evidence  of  lues  is  less  convincing  are  entitled 
to  the  benefit  of  the  doubt.  The  administration  of  mercury  and 
potassium  iodide  should  always  precede  the  exhibition  of  salvarsan, 
which  should  be  introduced  cautiously  and  in  small  doses,  which 
may  gradually  be  increased.  Success  in  securing  a  return  of  com- 
plete conductivity  has  been  reported  in  some  cases.  The  failure  of 
antisyphilitic  measures  to  restore  the  normal  function  does  not  prove 
that  the  scar  which  remains  may  not  have  been  of  syphilitic  origin. 

Nearly  all  grades  of  block  are  associated  with  a  greater  or  less 


27'J 


-f 


Figure  218 
November  20,   10.51  a.m.     Complete  block.     As  =  85;   Vs  =  46. 


1  f-ff         ♦»  ■  — ^  


Figure  219 

November  20,  10.56  a.m.     Delayed  conduction:  twenty-five  minutes  after  atropine  P-R 
interval  =  0.4    second.      As  =  85;    Vs  =  85. 


— - 

"-„                   "H 

-                              ! 

1                  1       " 

U. ...               ^ 

1 . . 

1 



S^*--^ 

•iflSSlff**^ 

i,Q,tStC. "' 

Figure  220 

November    20,    11.01    a.m.      Conduction  slow.     P-R  interval  =  0.22   second,   .4.$  =  85; 
Vs  -  85. 


.:_: — : :„:::i.      *  *  x        -    "H 

— «  5j     5  _ ««" ! ""  i . 


^jUi.Cvl^.^C'^w-^.,u--'^.i^c 


Figure  221 

November   20,    11.06  a.m.     P-R   interval  =  0.2   second:    As  =  So;    Vs  =  So. 
Complete   block    broken    by    tbe    administration    ot"    atropine. 


280  Treatment 

degree  of  cardiac  insufficiency.  Tin's  docs  not  necessarily  parallel 
the  severity  of  the  dissociation.  This  factor  requires  quite  as  much 
attention  as  the  block,  and  for  each  patient  appropriate  measures 
must  be  employed  to  improve  this  phase  of  his  difficulty. 

As  has  been  pointed  out  in  another  place,  the  activity  of  the 
vagus  is  sometimes  an  clement  in  producing  block.     Although   1 

believe  it  must  be  unusual  for  a  vagus  block  to  occur  without  other 
myocardial  defect,  it  should  always  he  taken  into  consideration  as 
a  possible  factor.  The  administration  of  atropine  may  he  used  to 
remove  vagUS  influences  and  thus  determine  their  relative  impor- 
tance. For  this  purpose  it  may  be  employed  subcutaneously  in 
closes  of  1.3  mg.  (1/50  grain).  Its  effect  should  be  apparent 
within  thirty  minutes.  The  effect  of  atropine  usually  disappears 
in  a  few  hours.  In  some  cases  it  is  desirable  to  continue  its  in- 
fluence  and  for  this  purpose  0.7  mg.  (1/100  grain)  may  be  given  by 
mouth  or  subcutaneously  at  six-hour  intervals  for  several  days. 
The  prolonged  administration  is  apt  to  cause  the  patient  considerable 
discomfort;  his  mouth  becomes  dry,  and  he  cannot  use  his  eyes  on 
account  of  the  loss  of  accommodation,  hence  its  use  must  be 
discontinued. 

Atropine  is  useful  to  counteract  the  effect  of  digitalis,  when  this 
has  been  given  to  a  point  where  its  toxic  effect  has  become  evi- 
dent through  the  development  of  heart  block.  Here  it  probably 
influences  only  the  vagus  part  of  the  digitalis  action. 

The  graphic  evidences  of  the  effect  of  the  administration  of 
atropine  are  shown  in  Figures  218,  219,  220  and  221.  These 
records  were  obtained  from  a  man  who  entered  the  hospital  with 
signs  of  marked  cardiac  insufficiency,  mitral  incompetence  and  a 
dilated  left  ventricle.  His  heart  was  rapid  and  rhythmic,  but 
showed  a  prolonged  conduction  interval  (P-R  =  0.2  second).  He 
was  given  digitalis  and  after  four  days  of  its  administration  the 
heart  suddenly  became  very  slow  (rate  46).  An  electrocardiogram 
taken  at  this  time  (Figure  218)  presented  the  evidences  of  a  com- 
plete heart  block.  He  was  given  1.3  mg.  atropine  subcutaneously, 
and  the  effect  is  shown  in  the  succeeding  records.  Figure  219,  taken 
twenty-five  minutes  after  the  atropine  was  given,  indicates  that 
there  is  no  longer  a  block,  although  the  conduction  time  is  very 
long  ( P-R  =  0.4  second)  and  the  ventricular  rate  has  increased  to 


Figure  222 

November   18,  3.40  p.m.     Complete  block.     Before  atropine.     As  —  y^;   Vszztf. 


-- 

. 

* 

—  - 

wfrfam&mfik 

: — 

o.a   s»v. 

-'— 

■_-_^_'_^_'_^^i^'_j_ ■ _-_-_'_d 

Figure  223 

November  18,  4.07  p.m.     Complete  block  twenty-five  minutes  after  atropine.     As  =  00; 
Vs  =  52. 


-  ; ; — — 



— IZ 



. 

....   , 



■ 



ml 

1 

*  T  ■ 

I  7; 

?t9t 

.  ^^ 

=z= 

— -— 

i^ 

0 

^J«, 

, 

Figure  224 

November     18,    4.10    p.m.       Complete    block.       As  =  100:     J's  =  6c 


' 

'"" . 

. 

-   - 





— 

.     _ 

, 1 

p 

>        ?!    ,- 

■p            t    B         V      -P"    T 

»  p 

■pi 

v    I 

4P          PI     » 

■p 

- 

■   '    '. 

_ 

. 

1    ' '_!' • 'j^ 

-  - 

/"  O  O •": 

O.X     J^c.    - 

■ 

_■- 

Figure  225 

November     iS,    4.1JP.M.      Complete    block       As _=  100;     f'j  =  60. 
A  case   of  block  not  removed  by   atropine  administration. 


282  Treatment 

85  per  minute.  Five  minutes  later  (Figure  220)  the  heart  rate 
had  not  changed,  hut  the  P-R  interval  was  reduced  to  0.22  second. 
Thirty-five  minutes  after  the  atropine  |  Figure  221  )  the  ventricu- 
lar rate  was  So,  the  P-R  interval  0.2  second.  This  was  the  maxi- 
mum atropine  effect,  which  gradually  whit  away  until,  at  the  end 
of  eight  hours,  complete  block  again  appeared. 

The  results  of  the  administration  of  atropine  to  another  patient 
with  a  complete  heart  block  (cause  unknown)  is  presented  in  Fig- 
ures ---,  223,  224  and  22^.  It  will  be  seen  that  atropine  did 
not  abolish  the  block  which  remained  complete  throughout  the  period 
of  observation.  It  did,  however,  cut  off  the  vagus  influences,  with 
the  result  that  both  the  auricular  and  ventricular  rates  were 
increased.* 

'Idle  question  of  the  administration  of  digitalis  to  patients  show- 
ing defects  of  the  property  of  conduction  must  be  studied  in  each 
individual,  To  many  showing  signs  of  cardiac  insufficiency  and 
dilatation,  its  use  is  beneficial.  In  eases  of  established  complete 
block,  it  is  not  eontraindicated  unless  it  produces  excessive  ven- 
tricular irritability  and  extrasystoles.  In  cases  of  delayed  conduc- 
tion, it  may  be  given  with  caution.  To  those  with  partial  block, 
it  is  usually  harmful.  Every  patient  with  conduction  defects  to 
whom  digitalis  is  given,  should  be  under  the  close  observation  of 
his  physician  until  its  effects  are  fully  established. 

EXTRASYSTOLES 

Our  present  knowledge  indicates  that  an  extrasystole  represents 

an  increased  irritability  of  some  portion  of  the  myocardium. 
Whether  this  is  due  to  a  chemical  alteration  of  the  muscle  cell,  histo- 
logical changes  in  the  cell  or  to  extracardial  nervous  influences 
which  increase  the  excitability  of  the  cell,  is  not  altogether  clear. 
From  the  evidence  at  our  disposal,  we  may  make  the  assumption 
that  in  different  patients  exhibiting  extrasystoles  the  cell  modi- 
fications are  not  necessarily  of  the  same  nature  and  that  in  one 
it  may  be  a  true  histological,  in  another  a  chemical  change  and 
in  a  third  a  nerve  influence.  The  object  of  therapeutic  measures 
is  to  reduce  the  myocardial  irritability  and  the  assumption  that  the 
change  in  this  property  may  be  the  result  of  such  diverse  influ- 

*Hart :  Amcr.  Jour.  Med.  Sc,  1915,  cxlix,  16. 


Treatment  283 

ences  afford  us  several  points  of  attack  which  may  be  considered 
in  each  case  according  to  its  individual  merits. 

There  are  certain  substances  which  have  an  undoubted  influence 
in  the  production  and  maintenance  of  extrasystoles.  They  prob- 
ably act  as  direct  toxins  to  the  myocardial  tissues.  These  arc  tea, 
coffee,  tobacco  and  certain  drugs,  such  as  digitalis,  theocin,  adrena- 
lin, chloroform,  etc.  The  reason  for  the  susceptibility  of  some- 
hearts  to  these  substances  is  entirely  unknown.  Some  individuals 
can  apparently  use  excessive  quantities  of  tobacco  with  entire  im- 
punity, while  in  others  a  small  amount  of  nicotine  will  produce  a 
high  degree  of  myocardial  irritability.  This  I  have  repeatedly  seen 
in  susceptible  individuals  who  have  been  closely  observed  to  deter- 
mine this  point.  In  the  same  way  certain  patients  show  a  similar 
tendency  with  digitalis  in  small  doses,  while  others  will  take  very 
large  amounts  without  evidence  of  increased  myocardial  irritability. 

The  first  attempt  to  reduce  the  excessive  cardiac  irritability  should 
consist  in  the  withdrawal  of  all  such  toxic  substances.  In  many 
instances  the  discontinuance  of  the  use  of  tea,  coffee  or  tobacco 
will  result  in  the  disappearance  of  extrasystoles,  in  others  the  cure 
is  not  so  simple,  but  it  is  not  fair  to  condemn  this  method  until 
it  has  been  given  a  prolonged  trial. 

Another  apparent  source  of  myocardial  irritability  is  an  abnor- 
mal condition  of  the  gastrointestinal  tract.  Whether  such  digestive 
disturbances  act  by  producing  substances  which  are  direct  toxins 
to  the  heart  muscle  or  by  purely  reflex  nervous  influences  is  not 
known,  but  it  seems  very  clear  that  in  a  certain  number  of  in- 
stances the  extrasystoles  will  disappear  with  a  correction  of  the 
gastrointestinal  disorder. 

It  is  also  wise  to  search  for  other  possible  sources  of  endogenous 
toxins  or  irritants  which  may  cause  an  abnormal  reflex  and  to 
remove  them  when  possible. 

A  distinction  should  be  made  between  the  extrasystoles  which 
are  associated  with  other  evidences  of  myocardial  damage  and  those 
which  occur  as  the  sole  evidence  of  disturbance  of  heart  function. 
In  the  former  case  our  treatment  may  be  mainly  directed  to  a 
correction  of  the  more  fundamental  cardiac  defect  and  often  the 
extrasystoles  will  become  less  evident  with  the  improvement  of 
the  other  features.     These  are  the  patients  in  whom  we  are  justi- 


284  Treatment 

Red  in  trying  the  effect  of  digitalis,  but  it  should  be  used  with 
care,  only  under  close  observation  and  should  be  discontinued  if 
it  increases  the  irritability  out  of  proportion  to  its  otherwise  bene- 
ficial effect.  In  those  in  whom  extrasystoles  are  the  only  sign  of 
abnormal  cardiac  activity,  digitalis  is  contraindicated ;  they  are 
often  made  worse  by  its  administration.  These  patients  should 
be  told  that  they  have  no  serious  heart  lesion,  they  should  not  cur- 
tail their  ordinary  physical  activities  and,  if  they  are  leading  a 
sedentary  life,  they  should  be  introduced  to  regular  exercise  in 
the  fresh  air  and  take  a  course  of  carefully  graduated  physical 
exercises,  which  in  a  very  large  number  of  instances  will  abolish 
the  extrasystoles  altogether.  I  know  of  no  drug  which  will  directly 
improve  the  cardiac  condition,  although  the  use  of  one  of  the  bro- 
mides or  valerian  may  be  of  service  in  tiding  over  a  period  of 
anxiety  and  apprehension. 

While  the  patient's  mind  should  be  put  at  rest  and  he  should  be 
reassured,  1  think  it  is  a  matter  of  some  importance  that  we  should 
get  rid  of  the  extrasystoles  if  we  can  by  the  simple  hygienic  meas- 
ures which  we  have  outlined  above.  I  have  the  impression  that 
by  allowing  extrasystoles  to  go  unchecked  the  abnormal  focus  in 
the  myocardium  acquires,  as  it  were,  a  habit  of  assuming  the  role 
of  pacemaker  for  the  heart,  and  this,  if  uncontrolled,  tends  to 
become  fixed  and  may  lead  to  the  development  of  abnormalities 
of  more  serious  moment. 

THE   ACCELERATE >    HEART 

In  seeking  methods  of  slowing  the  heart  that  is  beating  at  too 
rapid  a  rate,  we  should  always  endeavor  to  single  out  the  cog 
in  the  mechanism  which  is  defective.  When  the  demands  of  physi- 
cal exertion  exceed  the  capacity  of  the  heart  muscle,  it  must  be 
curtailed;  if  it  has  led  to  actual  heart  strain  and  dilatation,  the 
patient  must  be  put  to  bed  and  digitalis  may  be  found  of  benefit. 
[\  the  excessive  stress  arises  from  the  abnormal  functional  activity 
of  other  organs,  these  must  be  corrected  as  far  as  possible,  and 
during  the  process  the  heart  strength  must  be  conserved  by  rest. 
When  the  increased  rate  is  due  to  excessive  accelerator  influences, 
the  cause  may  often  be  found  in  the  deranged  function  of  some 
organ    remote    from    the   heart.      By    rectifying   this   disorder,   the 


Treatment  285 

abnormal  reflexes  will  be  excluded  and  the  tachycardia  will  dis- 
appear. In  these  conditions  sedatives,  such  as  the  bromides  and 
valerianates,  are  often  of  considerable  service. 

It  is  probable  that  by  far  the  greater  number  of  simple  tachy- 
cardias are  due  to  poisons  which  destroy  the  balance  of  the  extra- 
cardial  nerves  or  more  often  actually  increase  the  irritability  of 
the  sinus  node,  such,  for  example,  are  tea,  coffee,  tobacco,  alcohol, 
thyroid  extract  and  the  toxins  of  bacterial  infection.  The  indica- 
tion is  clear  that  the  absorption  of  these  substances  musl  be  cur- 
tailed and  their  elimination  facilitated.  Beyond  this,  rest  and  the 
application  of  cold  to  the  precordium  are  the  means  which  afford 
the  best  results.  Drugs  such  as  digitalis,  strychnine,  aconite,  etc., 
will  be  found  of  distressingly  little  value. 

PAROXYSMAL   TACHYCARDIA 

Since  our  conception  is  that  these  attacks  are  due  to  the  exces- 
sive irritability  of  some  point  in  myocardial  tissue,  which,  there- 
fore, assumes  the  role  of  a  pathological  pacemaker,  our  efforts  are 
directed  to  reducing  this  irritability  to  the  normal.  With  this  end 
in  view,  we  study  the  condition  of  the  heart  between  the  paroxysms 
and  correct,  as  far  as  may  be,  such  abnormal  functional  activities, 
adjusting  the  patient's  mode  of  life  to  the  amount  of  stress  which 
his  heart  is  able  to  support.  We  endeavor  to  remove  elements  which 
may  act  as  exciting  causes  to  the  paroxysm,  such  as  sudden  physi- 
cal exertion,  emotional  excitement  and  gastrointestinal  disturbances. 
We  put  the  patient  in  the  best  possible  physical  condition  in  the 
hope  that  the  attacks  may  be  less  frequent  or  that  he  may  be  better 
able  to  cope  with  the  paroxysms  when  they  arise.  When  the  attack 
comes  on,  the  patient  should  at  once  go  to  bed ;  this  they  usually 
do  without  advice,  but  exceptionally  one  sees  an  individual  who 
will  interrupt  his  activities  only  for  a  moment  at  the  beginning  of 
the  seizure  and  will  then  go  on  with  whatever  he  may  be  doing 
with   seemingly  little  discomfort. 

The  paroxysms  are  prone  to  terminate  spontaneously,  and  are  so 
variable  in  length  that  it  is  exceedingly  difficult  to  estimate  the 
value  of  measures  employed  to  arrest  them.  One  fact  is  very  cer- 
tain, we  have  no  one  single  means  which  invariably  stops  the  attacks. 
In  certain  individuals  the  attacks  can  be  stopped  by  various  muscu- 


286  Treatment 

lar  movements  or  by  assuming  some  special  posture.  The  patients 
themselves  will  often  discover  the  "trick"  by  which  this  end  is 
attained  or  the  physician  may  find  one  suited  to  the  patient's  needs 
by  testing  the  methods  which  have  proved  successful  in  others.     The 

following  are  a  few  of  the  means  which  may  be  tried:  holding  the 
breath  after  deep  inspiration;  strong  deglutition  movements  (as 
has  been  suggested  by  Vaquez,  this  may  be  accomplished  by  having 
the  patient  swallow  several  large  cachets  containing  some  inert  drug 
or  other  substance);  assuming  various  hodilv  attitudes,  such  as 
lying  on  a  couch  with  the  head  projecting  hcvond  the  edge  and 
thrown  hack  as  far  ;is  possible,  or  Hexing  the  head  forward  and 
bringing  it  down  between  the  legs  with  the  body  curled  up;  slap- 
ping tin-  chest;  a  long  drink  of  very  cold  water;  vomiting  induced 
by  tickling  the  pharynx  or  the  administration  of  an  emetic,  such  as 
mustard,  zinc  sulphate  or  the  syrup  of  ipecac;  cold  applications  to 
the  chest  wall.  It  is  probable  that  all  these  methods  act  by  stimu- 
lating the  vagus  either  by  mechanical  pressure  or  by  reflex  influ- 
ences. (  hie  can  frequently  stop  an  attack  temporarily,  sometimes 
permanently,  by  direct  vagus  pressure.  This  is  accomplished  by 
making  digital  pressure  over  the  carotid  sheath  just  below  the  angle 
of  the  jaw.  Right  vagus  pressure  is  usually  much  more  efficacious 
than  left  vagus  pressure  (see  Figures  152  and  153):  the  nerves 
should  he  manipulated  one  at  a  time,  compression  should  never  he 
applied  to  both  vagi  at  the  same  moment,  as  there  is  a  possibility 
of  causing  serious  arrest  of  the  heart.  Ocular  pressure  may  he 
tried,  hut  it  is,  as  a  rule,  less  effective  than  vagus  pressure. 

Digitalis  is  of  little  or  no  value  in  the  short  paroxysms,  hut  in 
attacks  lasting  several  days  it  may  be  pushed  to  the  physiological 
limit.  In  the  tachycardias  of  auricular  origin  we  may  hope  to 
induce  an  A-V  block;  in  those  rare  paroxysms,  which  arise  from  a 
focus  in  the  wall  of  the  ventricle,  digitalis  is  contraindicated. 

The  intravenous  use  of  crystalline  strophanthine  has  been  found 
succe>>ful  in  arresting  the  paroxysms  on  a  number  of  occasions. 
A  single  dose  of  one-half  milligram,  dissolved  in  8,000  parts  of 
normal  saline,  may  be  given.  This  dose  may  he  repeated  after  an 
interval  of  twenty-four  hours. 

No  one  of  the  above  measures  is  always  successful.  Some 
paroxysms   resist  all  the  attempts  made  to  arrest  them   and   ulti- 


Treatment  287 

mutely  stop  spontaneously.     Under  these  circumstances  the  patient 

must  be  made  as  comfortable  as  possible  I  te  is  allowed  to  assume 
the  posture  in  which  he  is  most  at  case.  Quiet  and  resl  are  attained 
by  the  administration  of  bromides,  valerian,  or,  in  conditions  of 
great  distress  and  restlessness,  a  hypodermic  of  morphine.  There 
is  a  long  list  of  drugs  which  have  been  reported  to  be  efficienl  in 
stopping  the  attacks,  among  these  are  aconite,  amy]  nitrite,  strych- 
nine, veratrine,  hypophysis  extract,  etc.,  etc.  These  probably  are 
without  any  real  effect  and  owe  their  reputation  to  the  coincidence 
of  their  administration  with  the  time  of  the  spontaneous  termina- 
tion of  the  paroxysm. 

SINUS  ARRHYTHMIAS 

We  have  seen  that  cardiac  irregularities  arising  in  the  sinus  node- 
are  due  to  a  condition  of  the  nodal  tissue  which  makes  it  peculiarly 
susceptible  to  vagus  influences.  When  the  rhythmic  changes  are 
synchronous  with  the  respiratory  movements,  we  may  regard  them 
as  entirely  physiological,  and  as  such  they  require  no  treatment. 
They  do  not  indicate  an  abnormal  condition  of  the  myocardium, 
hence  there  is  no  reason  for  subjecting  the  individual  presenting  this 
irregularity  to  unusual  restrictions  or  for  limiting  his  accustomed 
activities. 

The  irregularities  of  simts  origin,  which  are  independent  of  the 
respiratory  movements,  have  a  somewhat  different  significance. 
Here,  I  believe,  that  the  cause  of  the  instability  of  the  nodal  tissue 
is  usually  a  true  myocardial  defect  of  which  the  functional  change 
of  the  sinus  nbde  is  often  the  earliest  evidence.  It  is  certainly 
wise  that  these  patients  should  be  closely  watched,  with  the  pur- 
pose of  detecting  at  the  earliest  possible  moment  further  signs  of 
myocardial  damage,  should  these  present.  In  themselves,  these 
irregularities  are  of  little  consequence ;  they  do  not  demand  treat- 
ment. These  patients  never  show  cardiac  insufficiency  without  pre- 
senting signs  of  abnormalities  of  the  heart  other  than  this  arrhyth- 
mia. When  the  irregularity  is  first  discovered,  the  patient's  activ- 
ities should  be  moderately  restricted,  in  order  that  the  heart  may 
not  be  subjected  to  any  considerable  stress  pending  the  determina- 
tion of  the  extent  of  the  myocardial  damage.  If  at  the  end  of  a 
reasonable  period  it  appears  that  the  irregularity  is  the  only  evi- 


288  Treatment 

dence   of    disturbed    function,   the    restrictions   may   be   gradually 
relaxed. 

AURICULAR    FLUTTER 

Auricular  flutter  indicates  an  exceedingly  irritable  condition  of 
the  auricle,  which  is  contracting  rhythmically  at  a  very  rapid  rate. 
It  is  usually  associated  with  a  defect  in  the  .-/-/'  junctional  tissues, 
so  that  a  part  of  the  auricular  impulses  are  blocked  and  the  ven- 
tricle responds  only  to  every  other  stimulus  originating  in  the  upper 
chamber.  Hence  the  object  of  our  therapeutic  measures  is  first  to 
increase  the  degree  of  block  and  thus  reduce  the  number  of  the 
auricular  stimuli  which  are  able  to  reach  the  ventricle,  and,  second, 
to  diminish  the  irritability  of  the  auricular  tissues  so  that  the  sinus 
may  regain  its  ascendency  and  resume  its  role  of  cardiac  pacemaker. 

During  the  attack  the  patient  should  be  in  bed  and  as  nearly 
horizontal  as  possible.  Frequently  the  patient  breathes  more  easily, 
if  the  head  is  somewhat  elevated,  and  during  urgent  dyspncea  it 
may  be  necessary  to  allow  him  to  sit  up  in  a  chair.  He  must  be 
kept  as  quiet  as  possible  and  all  friends  and  sources  of  emotional 
excitement  must  be  excluded.  Sleep  and  rest  may  be  secured  by 
the  administration  of  bromides  and  valerian  or  even  morphine,  if 
the  restlessness  is  excessive.  Food  should  be  given  frequently  in 
small  amounts  and  in  an  easily  digested  form.  As  a  rule,  large 
amounts  of  fluid  should  be  avoided. 

As  in  the  case  of  "paroxysmal  tachycardia,"  which  seems  to  bear 
a  very  close  relationship  to  auricular  flutter,  stimulation  of  the 
vagus  will  sometimes  slow  the  ventricles  and  even  arrest  the 
paroxvsm.  A  number  of  methods  for  attaining  this  result  have 
been  detailed  on  page  286,  and  need  not  be  repeated  here.  The 
effect  of  vagus  stimulation  is,  however,  usually  transitory  and  is 
unreliable  as  a  lasting  therapeutic  measure.  On  theoretical  grounds 
the  stimulation  of  the  left  vagus  should  have  a  greater  effect  in 
slowing  the  ventricles,  while  the  right  vagus  should  better  control 
the  auricular  tachycardia.  That  this  is  not  always  the  case  is  shown 
in  Figures  226  and  227.  These  are  portions  of  records  secured 
from  a  man  of  forty-nine  during  an  attack  of  auricular  flutter  last- 
ing several  days.  His  auricles  were  contracting  at  a  rate  of  300 
per  minute;  his  ventricular  rate  was  150  per  minute.  At  the  point 
in  Figure  226  indicated  by  the  arrow,  digital  pressure  was  made 


289 


"""TTT]?J3i 


—  2 

v  -j. 


—  |j 


*> 

». 

or^ 

, 

2(p  Treatment 

on  the  right  vagus  nerve  and  continued  for  ten  seconds.  During 
this  time  the  ventricles  did  not  contract,  the  auricular  activity  was 
not  affected.  <  >ne  second  after  pressure  was  discontinued  the  ven- 
tricles resumed  their  contractions  at  a  rate  of  25  per  minute.  This 
rate  gradually  increased  and  at  the  end  of  five  minutes  the  ven- 
tricular rate  had  returned  to  150.  The  effect  of  left  vagus  pres- 
sure is  shown  in  Figure  227.  Mere  again  it  is  evident  that  the 
auricular  tachycardia  is  unchanged.  There  was  a  ventricular 
escape  at  the  end  of  2.4  seconds  and  the  intervals  rapidly  short- 
ened and  a  ventricular  rate  of  [50  per  minute  was  attained  in  nine 
seconds,  while  vagus  pressure  was  still  being  made. 

The  drugs  which  are  of  most  value  in  auricular  flutter  are  digi- 
talis and  others  belonging  to  this  group.  The  ohject  to  he  sought 
is  an  increase  in  the  degree  of  auriculo-ventricular  block,  so  that 
a  portion  of  the  impulses  originating  in  the  irritable  auricle  may 
be  obstructed  and  the  ventricular  rate  reduced.  In  order  to  secure 
a  prompt  effect  digitalis  must  be  administered  in  large  doses.  It 
may  be  given  subcutaneously  if  the  patient  is  in  great  distress,  or 
if  immediate  relief  is  demanded  strophanthin  may  be  given  intra- 
venously, observing  the  pracautions  that  have  already  been  sug- 
gested in  the  use  of  this  powerful  alkaloid.  Exhibited  by  mouth 
in  full  doses,  digitalis  may  require  several  days  to  reduce  the  ven- 
tricular rate  to  the  normal,  but  a  considerable  slowing  is  usually 
seen  in  forty-eight  hours.  When  the  ventricular  rate  reaches  about 
70  per  minute,  although  the  auricles  are  usually  still  in  a  condi- 
tion of  flutter,  the  digitalis  may  be  stopped,  in  the  hope  that  a 
physiological  rhythm  may  be  recovered.  If  the  ventricle  shows  a 
tendency  to  increase  its  rate,  digitalis  should  be  resumed.  It  is 
quite  probable  that  soon  after  this  the  auricles  will  begin  to  fibril- 
late,  but  often  the  physiological  rhythm  will  reappear  with  no 
intervening  period  of  fibrillation.  The  question  has  been  debated 
as  to  whether  the  fibrillation  is  due  to  the  administration  of  the 
digitalis.  This  seems  quite  probable,  hence  it  would  seem  wise  to 
employ  this  drug  only  to  a  point  where  it  controls  the  ventricular 
rate  within  reasonably  normal  limits,  and  from  time  to  time  to 
discontinue  it,  carefully  observing  the  functional  condition  of  the 
heart. 

A  typical  favorable  reaction  to  digitalis  is  shown  in  Figures  228, 


FlGURE  228    April   6.      Refore   treatment.      Auricular  flutter   with    irregular   ventricular 
contractions    150   per   minute. 


m_u.l:.l  I :  "rn~T 


- nst- 


- 


----- 


FIGURE  229       April  9.     Ventricle  irregular  rate   100. 


Z=^:: ■—'-     I  -  ■  :      —  '^— 4—   l  I  II  I  -     i  -       •         I  !  I  '  :  ■    ■  : 


FlGURE  230    April   15.      Ventricle  regular,   rate   75.     Auricles   still   in   flutter.      After 
this   digitalis  was  stopped. 


FlGURE   2  31       April  22.     Regular  sequential   rhythm.     Auricular  flutter  has  stopped. 
The  above   four  records  show   the  effects   of   well-regulated   digitalis  administration  in 
a  case   of  auricular  flutter. 


_•.,_•  Treatment 

229,  230  and  231.  '  'n  April  6,  before  treatment  |  Figure  228),  the 
ventricular  rate  was  150  per  minute;  under  large  doses  <>i"  digitalis 
the  rate  was  reduced  to  100  (Figure  229).  The  quantity  of  digi- 
talis was  then  reduced,  and  <>n  April  13  the  activity  was  that  pre- 
sented in  Figure  -'^o.  The  auricles  wire  still  in  flutter,  with 
rhythmic  contractions  at  the  rate  of  about  300  per  minute;  the 
ventricles  were  also  perfectly  rhythmic,  but  responded  only  to  every 
fourth  auricular  impulse.  At  this  point  digitalis  was  discontinued 
and  a  few  days  later  the  heart  returned  to  a  sequential  rhythm 
(  Figure  231).  At  no  period  was  auricular  fibrillation  observed  in 
this  patient. 

Ah' Hit  one-half  of  the  cases  of  auricular  flutter  recover  a  physio- 
logical rhythm,  many  of  them  pass  into  auricular  fibrillation  and, 
in  a  considerahle  number,  this  is  continued  for  the  remainder  of  life. 

The  use  of  potassium  iodide,  in  association  with  digitalis,  has 
given  favorable  results  in  some  cases.*  It"  there  is  evidence  of  a 
syphilitic   infection,  a   course  of   mercury   and   iodide   is   indicated. 

AURICULAR  FIBRILLATION 

It  is  most  generally  held  that  this  condition  is  caused  by  a  highly 
irritable  condition  of  the  auricular  wall.  The  disturbances  of  the 
circulation  are  almost  entirely  due  to  the  secondary  effects  on  the 
ventricles,  which  are  induced  by  the  abnormal  stimuli  showered 
upon  the  junctional  tissues  by  the  frenzied  activity  of  the  auricles. 
The  purpose  of  treatment  is,  therefore,  to  reduce  the  irritability 
of  the  auricles,  in  the  hope  of  securing  coordinated  contractions  of 
the  auricular  muscle.  Failing  in  this,  we  should  attempt  to  obstruct 
a  portion  of  the  impulses  set  free  in  the  upper  chamber  and  thus 
relieve  the  ventricles  of  the  stimuli,  which  lead  to  such  rapid  and 
ineffectual  contractions. 

Our  means  to  reduce  the  excitability  of  the  auricular  muscle  are 
limited  and  most  often  unavailing,  yet  I  believe  that  in  every  case 
of  auricular  fibrillation  discovered  near  the  time  of  the  inception 
of  the  new  rhythm,  an  attempt  should  he  made  to  bring  the  auric- 
ular activity  hack  to  the  normal.  It  has  been  pointed  out  that 
.-1  sudden  increase  in  intra-auricular  pressure  is  probably  an  impor- 
tant factor  in  inducing  the  onset  of  fibrillation  in  a  heart  previously 

♦Ritchie:   Auricular  Flutter,   1914,  p.   132. 


Treatment  293 

damaged  by  disease.  Anything  which  we  can  do  to  prevenl  venous 
congestion  and  overfilling  of  the  auricles  of  a  hearl  in  which  we 

suspect  myocardial  defects,  should  be  employed  as  a  prophylactic 
against  fibrillation.     It"  fibrillation  has  commenced,  resl  in  bed  is  at 

once  indicated,  and  in  cases  with  evident  venous  stasis  and  over- 
distension of  the  auricles,  a  prompl  phlebotomy  may  sometimes 
relievo  the  increased  pressure  and  permit  the  auricle  to  resume  a 
physiological  activity.  The  active  elimination  of  the  toxins  of  the 
acute  infections  or  of  other  poisons  may  be  accompanied  by  the  reap- 
pearance of  normal  auricular  contractions,  if  the  ventricular  rate 
becomes  very  rapid,  digitalis  may  be  employed  in  full  doses  until 
the  ventricles  are  slowed  to  about  90  a  minute,  but  it  should  then 
be  discontinued,  for  digitalis,  undoubtedly,  has  the  effect  of  increas- 
ing the  irritability  of  the  muscle  cells  of  the  heart,  and  in  these 
early  cases  it  is  wise  to  remove  this  influence  in  the  hope  that 
the  auricles  may  recover  their  normal  coordinated  contractions. 

As  has  already  been  stated,  our  efforts  to  reduce  auricular  excita- 
bility and  to  secure  a  return  to  a  normal  rhythm  are  usually  unsuc- 
cessful, auricular  fibrillation  becomes  established  and  will  probably 
continue  to  the  end  of  life.  It  is  in  these  cases,  however,  that 
the  treatment  of  abnormal  myocardial  function  obtains  its  most 
brilliant  successes. 

The  attention  of  the  physician  must  be  centered  on  the  ven- 
tricular activity,  if  the  rate  of  the  lower  chamber  is  not  over  75 
per  minute,  and  the  heart  is  well  compensated  little  need  be  done 
for  the  patient  other  than  to  see  to  it  that  his  mode  of  life  con- 
forms to  the  limited  amount  of  force  which  such  a  heart  has  in 
reserve.  Physical  and  emotional  strain  must  be  avoided,  the  exces- 
sive use  of  tobacco,  alcohol,  tea  and  coffee  are  forbidden,  gastro- 
intestinal disturbances  must  be  corrected  and  exposure  to  infections 
shunned. 

With  a  more  rapid  and  irregular  ventricular  rate,  the  indica- 
tions for  treatment  are  quite  different.  The  patient  should  be  put 
to  bed  at  once  and  kept  as  quiet  as  possible.  Food  should  be  given 
at  frequent  intervals  in  easily  digested  forms,  the  amount  of  fluids 
taken  should  usually  be  restricted.  Rest  may  often  be  secured 
by  one  of  the  simple  hypnotics,  veronal,  trional,  etc.  The  most 
important  object  to  be  attained  is  to  block  a  portion  of  the  hap- 


294  Treatment 

hazard  auricular  impulses,  so  that  these  may  erase  to  vex  the  over- 
acting ventricles.  This  can  nearly  always  be  secured  by  the  admin- 
istration of  digitalis  or  strophanthus.  In  a  considerable  number 
nt"  these  hearts  the  myocardial  damage  is  not  limited  to  the  auric- 
ular wall,  but  has  also  involved  the  ./-/'  bundle.  This  makes  them 
peculiarly  susceptible  t<>  digitalis  influences,  and  with  this  drug 
it  is  usually  easy  t<>  produce  a  considerable  degree  of  auriculo- 
ventricular  block.  While  rest  in  bed  is  essential  to  the  successful 
treatment  of  these  cases,  it  is  quite  easy  to  demonstrate  thai  this 
alone  is  not  sufficient,  in  the  majority  of  instances,  to  reduce 
the  ventricular  rate  to  the  desired  point,  outside  demands  in  ex< 
of  the  functional  capacity  of  the  heart  are  only  partly  responsible 
for  the  increased  rale.  This  is  due  in  a  very  large  degree  to  the 
abnormal  auricular  activity  and  until  this  influence  is  checked  the 
ventricles  cannot  be  satisfactorily  controlled.  Hence,  the  admin- 
istration of  digitalis  is  practically  always  a  necessity. 

1  low  much  digitalis  must  we  give?  This  question  can  be  answered 
only  by  studying  the  individual  patient.  We  must  give  it  in  suffi- 
cient amounts  to  secure  its  physiological  effects,  and  this  can  be 
determined  only  by  observing  the  reaction  of  each  heart  to  the 
drug   during   its   administration. 

The  method  which  I  have  found  most  satisfactory  is  to  begin 
by  giving  by  mouth  a  good  infusion  or  the  tincture.  I  use  30  c.c. 
(i  ounce)  of  the  infusion  or  4  c.c.  (no  minims)  of  the  tincture 
in  each  twenty-four  hours  until  a  definite  physiological  effect  is 
observed.  This  is  usually  seen  in  from  three  to  five  days.  The 
beneficial  effects  of  rest  and  the  administration  of  digitalis  arc 
shown  in  the  graphic  records  of  the  brachial  pulse,  taken  at  inter- 
vals of  two  or  three  days  from  a  single  patient  (  Figures  232,  233, 
234,  235,  236  and  237).  I  think  the  hest  method  for  watching  the 
effect  of  the  drug  is  to  make  frequent  estimations  of  the  apex 
rate,  the  radial  rate  and  the  pulse  deficit,  as  described  in  the  chap- 
ter on  auricular  fihrillation  (page  164).  When  the  rate  of  the 
heart,  determined  by  auscultation  over  the  apex,  falls  below  90 
and  the  pulse  deficit  is  less  than  10,  the  dosage  may  he  gradually 
diminished,  hut  should  he  continued  in  sufficient  amount  to  effect 
a  still  further  slowing  of  the  heart  and  a  diminution  in  the  pulse 
deficit.     As  a   rule,    I    find  that   these   hearts  are  most   efficient   if 


295 


FIGURE  2^3         January  25.     Rate  115. 


FIGURE  235        January   29.     Rate   96. 


FIGURE  237  February   5.      Rate   54. 

A  series  of  records  taken  from  a  case  of  auricular  fibrillation  showing  the  progressive 
effect   of   digitalis   administration. 


296  Treatment 

the  rate  is  kepi  between  00  and  70  per  minute  with  no  deficit. 
When  patients  are  observed  in  this  way,  it  is  very  rare  to  see  the 
disagreeable  toxic  effects  formerly  so  common  in  digitalis  therapy; 
nausea  and  vomiting  are  very  infrequent,  and  it  is  almost  never 
necessary  to  discontinue  the  drug  on  account  of  these  symptoms. 
Excessively  slow  rates  and  the  "coupled  rhythm"  are  so  unusual 
that  they  are  curiosities.  Notwithstanding  the  infrequency  of  the 
development  of  the  signs  of  digitalis  intoxication  in  patients  to 
whom  the  drug  is  administered  by  this  method,  they  occasionally 
arise  and,  should  the  heart  rate  fall  below  50  or  the  "coupled 
rhythm"  appear,  digitalis  must  he  stopped  at  once.  When  the  rate 
has  increased  to  70,  digitalis  should  he  resumed  in  a  smaller  dose. 
The  patient  should  he  kept  in  hed  for  a  week  after  the  rate  has 
reached  70.  He  may  then  hi-  allowed  to  slowly  resume  his  activ- 
ities. Any  notable  acceleration  of  the  heart  or  increase  in  the 
pulse  deficit  is  a  warning  that  he  is  exceeding  the  stress  which 
his  myocardium  may  safely  support  and  his  exertions  must  he 
correspondingly  reduced.  It  is  usually  necessary  to  continue  small 
doses  of  digitalis  for  an  indefinite  period.  I  have  patients  who 
have  not  missed  their  daily  dose  of  digitalis  for  five  years. 

If  the  physical  exertion  is  increased  very  cautiously  and  the  heart 
rate  is  not  allowed  to  exceed  70  a  minute,  hypertrophy  will  grad- 
ually develop  and  in  some  individuals  the  myocardium  will  recover 
an  extraordinary  capacity  for  work-. 

While  a  majority  of  those  suffering  from  auricular  fibrillation 
respond  to  a  course  of  treatment  as  outlined  above  in  a  satis- 
factory manner,  there  are  some  who  are  exceedingly  difficult  to 
handle.  These  are  usually  cases  of  long-standing  fibrillation  which 
have  been  untreated,  or  those  who  have  been  treated  intermittently 
with  intervening  periods  of  cardiac  decompensation.  They  usually 
present  evidences  of  extensive  myocardial  damage  extending  into 
the  ventricular  tissues  and  often  show  frequent  ventricular  extra- 
systoles.  The  polygrams  of  such  a  case  are  shown  in  Figures  238, 
239  and  240.  The  effect  of  digitalis  in  these  cases  is  to  cause  a 
great  increase  in  the  number  of  ventricular  extrasystoles  without 
materially  slowing  the  ventricular  rate.  Figure  239  shows  the 
record  obtained  on  the  second  day  of  the  administration  of  our 
usual  initial  dosage  of  digitalis.    On  account  of  the  coupled  rhythm, 


2<j7 


Jtlgulaf 


a 


Figure  238 
Patient    "J.    M."      Auricular    fibrillation.      Record    on    admission    to    the    hospital 
October  2. 


Jugular 


Brachial 


0.2   second 


Patient    "J.    M." 
digitalis  in  two  days. 


Figure  239 
October    14.      Result   of    the   administration    of 
"Coupled  rhythm." 


cc.    tincture    oi 


Jugular 


Brachial 


Figure  240 

Patient  "J.   M."  November  22.     Result  of  the  administration  of  6  cc.  of  the  tincture 
of  digitalis  in 'three  davs.     Everv  other  ventricular  contraction  is  an  extrasystole. 
A  case  of  auricular  fibrillation  which  reacted  unfavorably  to  digitalis. 


Treatment 

the  drug  was  at  once  discontinued,  the  pulse  remained  rapid,  but 
the  extrasystQles  disappeared,  and  five  weeks  later  an  attempt  was 
again  made  to  give  digitalis,  bul  in  a  smaller  dose.  After  four 
days  the  coupled  rhythm  reappeared  i  Figure  240).  Through  rest, 
bromides,  aspiration  of  chest  fluid  and  diuresis  this  head  was  finally 
improved  so  that  it  tolerated  small  doses  of  digitalis,  and  the 
patient  was  eventually  able  to  leave  the  hospital  and  resume  Ins 
occupation  of  watchman. 

Each  time  that  the  ventricles  are  allowed  to  become  rapid  and 
the  heart  to  become  insufficient,  it  will  be  found  more  difficult  to 
control  the  rate  and  secure  a  fair  degree  of  compensation,  and 
when  to  this  is  added  a  myocardial  irritability,  which  is  excessively 
increased  by  digitalis,  it  will  require  all  the  ingenuity  of  the  physi- 
cian to  devise  means  to  obtain  an  improvement  in  the  cardiac 
function. 

<  Occasionally  one  sees  a  patient  whose  condition  is  so  grave  that 
some  immediate  means  must  he  employed  to  reduce  the  excessive 
heart  rate.  In  these  one  sometimes  can  obtain  almost  miraculous 
results  by  the  intravenous  administration  of  strophanthin ;  this 
should  never  be  given  if  the  patient  has  been  recently  taking  digi- 
talis or  strophanthus  in  any  form. 

When  there  is  a  history  of  a  syphilitic  infection  and  a  positive 
Wassermann  reaction,  these  patients  should  always  be  give^i  a  course 
of  antisyphilitic  treatment. 

Figure  241  is  the  record  of  a  case  of  auricular  fibrillation  three 
days  after  digitalis  was  commenced;  two  days  later  the  pulse  sud- 
denly became  very  slow  and  on  listening  at  tin-  apex  the  coupled 
rhythm  could  he  detected.  The  electrocardiogram  taken  at  thi< 
time  (Figure  -'4-' )  indicated  that  the  slow  pulse  rate  was  due  to 
a  complete  heart  block,  associated  with  ventricular  extrasystoles, 
which  were  too  weak  to  show  in  the  peripheral  arteries. 

In  Figures  243,  244,  245  and  246  are  presented  a  series  of 
records  taken  from  a  patient  during  a  course  of  digitalis  treat- 
ment. On  April  12  (Figure  213)  the  rate  was  138;  three  days 
later  (  Figure  2_p4)  this  was  reduced  to  100  heats  per  minute.  (  >n 
April  18  (Figure  245)  the  rate  fell  to  ^J  and  the  increased  irri- 
tability of  the  ventricle  was  evidenced  by  the  occasional  appear- 
ance of  extrasystoles.     At  this  time  digitalis  was  discontinued  and 


Auricular  Fibrillai  eon 


299 


cardii  : 


days. 


Figure  241 

Patient    "G."      Auricular    fibrillation.      Rate    104.      Digitalis   had   been   taken   for   two 


H 


T     A. 


pw 


ww^   r\+mmm 


Jugular 


Electro- 
cardiogram 


Brachial 


Figure  242 

Patient  "G."      Fourth   dav  of   digitalis   therapy.      Note    •'coupled   rhythm,"   every   other 
ventricular  contraction  is  an  extrasystole  which  does  not  affect  the  jugular  or  the  brachial 

pressures. 


300  I'ki  \i  mi  \  i 

on  May  4  (Figure  J40)  extrasystoles  had  completely  disappeared 
and  the  heart  rate  was  94  per  minute.  'This  series  ol  records  also 
shows  the  influence  of  digitalis  in  modifying  the  form  of  the  T 
wave. 

The  effect  of  digitalis  on  blood-pressure,  in  auricular  fibrillation, 
has  long  been  a  matter  of  contention.  Thirty  years  ago  it  was 
thought  that  the  administration  of  digitalis  elevated  blood-pressure, 
but  this  view  was  controverted  by  many  subsequent  observers,  such 
as  Christeller,  Frankel,  Ileike,  Hansen,  Gross,  Potain,  and  others. 
Their  opinions  have  been  summarized  by  Janeway,*  who  says: 
"All  of  the  above  observers  fail  to  find  any  relation  between  the 
arterial  tension  and  the  circulatory  improvement    from  digitalis." 

Our  present  evidence  justifies  us  in  asserting  that  in  the  cases 
of  cardiac  insufficiency,  where  digitalis  is  of  most  value,  it  raises 
blood-pressure  by  slowing  and  increasing  the  force  of  ventricular 
activity. 

The  failure  of  former  observers  to  recognize  this  fact  was  de- 
pendent on  two  elements:  (1)  That  it  was  not  then  known  that 
the  benefits  of  digitalis  administration  are  mainly  evident  in  cases 
of  auricular  fibrillation,  and  (2)  that  they  had  no  satisfactory 
method  of  estimating  the  blood-pressure  in  these  cases,  in  which 
the  successive  contractions  of  the  heart  vary  so  greatly  in  force 
and  time.  Mackenzie  says,  in  his  "Monograph  on  Digitalis":  "In 
our  observation,  even  when  the  drug  was  pushed  and  caused  nausea 
and  heart  irregularities,  we  could  detect  no  appreciable  effect  upon 
the  blood-pressure   (except  in  one  case)." 

Since  we  have  come  to  recognize  that  digitalis  finds  its  chief 
usefulness  in  cases  of  auricular  fibrillation,  and  have  applied  our 
method  of  estimating  the  ''average  systolic  blood-pressure"  to  the 
study  of  this  group,  it  has  become  clear  to  us  that  hand  in  hand 
with  the  improvement  in  the  patient's  condition  the  average  sys- 
tolic blood-pressure  is  elevated. 

This  is  best  made  evident  by  the  presentation  of  several  charts, 
which  have  been  selected  from  a  considerable  number,  all  ot  which 
show  the  same  features. 

figure  [26  shows  the  effect  of  rest  and  digitalis  on  a  case  under 
observation  in  the  Presbyterian  Hospital  for  two  weeks.    The  dimi- 

*The  Clinical  Study  of  Blood-pressure,  New  York,   1904,  p.  210. 


JOl 


- 


Figure  243      April  15.  Rate  i*8. 

(The    "   control   curve"    was   made    artificially    to  standardize    the    galvanometer    string 

by    introducing    one     millivolt     of    current     into    the  circuit.       All     of     tin-     recordf 
standardized   in   this  way.) 


z=z. 

—  1    1    \-_  • 

BE 

!Er 

H 

-  ,  1        1  .:iri~' '  1    1  — ■ — 

-     ;       :         _ 

Figure  244     April   15.     Rate   100. 


FIGURE  24^       April    18.       Rate  57.     Ventricular  slowing,  appearance  of  extrasystoles  and 
change  in  form  of   T  wave. 


FIGURE  246        May  4.     Rate  94.     Digitalis  stopped  on  April   19. 
Effect  of  digitalis  in  a  case  of  auricular  fibrillation. 


3<>2  Treatment 

nution  in  the  deficit  and  the  gradual  increase  in  the  average  sys- 
tolic blood-pressure  is  quite  clear.     During  this  period  all  of  the 

patient's  symptoms  improved,  and  she  was  able  to  leave  the  hos- 
pital to  return  to  her  home. 

ddiis  chart  also  shows  how  misleading  would  have  been  the  sys- 
tolie  blood-pressure  estimations  made  by  the  ordinary  method  (see 
figures  at  the  bottom  of  the  chart),  for  at  these  brachial  pres- 
sures only  four  or  five  waves  per  minute  reached  the  radial  during 
the  three  days  following  her  admission.  The  diagram  indicates 
that  the  full  digitalis  effect  is  not  obtained  for  four  or  five  days; 
this  we  have  found  to  be  quite  usual. 

Figure  247  is  the  chart  of  a  man  who,  during  the  whole  period 
of  observation,  insisted  upon  following  his  ordinary  occupation.  1  le 
was  not  confined  to  bed  at  any  time,  although  we  should  have 
considered  this  the  wisest  course  when  he  was  first  seen.  He, 
therefore,  illustrates  the  effect  of  digitalis  independent  of  the  influ- 
ence of  any  considerable  amount  of  rest  in  the  horizontal  position. 
The  rise  in  blood-pressure  coincident  with  a  slowing  of  the  pulse 
and  diminishing  deficit  and  the  fall  of  pressure  corresponding  to  an 
increase  in  the  pulse  rate  and  deficit  stand  out  clearly.  The  observa- 
tions cover  a  period  of  nineteen  months,  and  the  changes  in  the 
deficit  and  the  blood-pressure  could  be  closely  correlated  with  his 
other  symptoms.  Whenever  there  was  any  considerable  deficit  or 
the  blood-pressure  fell  this  wTas  associated  with  more  or  less  dysp- 
noea, a  lack  of  vigor  and  feelings  of  lassitude. 

Figure  248  is  that  of  a  woman  who  was  in  the  Presbyterian 
Hospital  during  the  whole  period  of  observation  as  represented  by 
the  diagram.  The  initial  deficit  on  admission,  which  showed  a 
marked  and  sudden  diminution  with  the  administration  of  a  freshly 
made  infusion  of  digitalis  (an  ounce  was  given  on  October  17), 
the  first  setback  induced  by  getting  out  of  bed,  her  subsequent  im- 
provement under  rest  and  digitalis,  the  second  setback  brought  on 
by  an  attack  of  hemorrhoids  and  the  variations  in  blood-pressure, 
associated  with  the  various  stages  of  her  progress,  are  all  indicated 
in  a  graphic  manner. 

ALTERNATION 

is  a  positive  indication  for  limiting  the  work  which  the  heart  is 
called   upon  to  perform.     Although   we  may   not  as  yet   agree  to 


Treatment 


3"3 


"  Aprlltfiy                                 *»"«          "<*■            """• 

c    i     il      a     J      £ 
Dn.     J»nT'h.     M»r.            »f»r              4    -.    -     •/.     o    ir 

N     1     1     1     II   inUII    I    12          8    12  21    4 

II    IH  25  1(1  <U  20    *    17    2    It  U    4     17  2»  13  25   11  28     t     I 

1 

I                          j 

130  I 

180  f 
HO  I 
100  Ij 
90- 
80  " 

Wk                                                    i<           /- 4                  ?  J< 
sWlK                 •   ▲  7         V 

^H_______~  -^                        ■  ________    -  _. 

70 - 

IfW^k  ^^  ^\) 

r t  1-^Sik"   i-^TH"-^''  !    \    /  ' 

60 

j 

i  ^s      r                                      v/^k  * 

o..  J 

-   S/-4-                                                            .    <V^' 

50 

_L                                                         _  .     _ . 

t:::: ±±±±±±±4:4:111: 

T 

ri l±1±±±a.x+±±± 

OlOtTAt. 

ISO    45   45    45  46  -45    45    45   (0     0           20   30   20   20 

0    10   20    20    20   20    20    20    20    20    20   20    10    30     10    M    11      0     14    14 

Figure  247 

The  shaded  area  represents  the  pulse  deficit;  the  upper  edge  is  the  apex  rate;  the 
lower  edge  the  radial  rate.  The  hroken  line  is  the  "average  systolic  blood  pressure."  The 
figures  in  the  digitalis  column  indicate  minims  of  the  tincture  per  day.  Patient  not 
confined   to   bed. 


0«L                                                          !»o 

».                                              n«f 

„,„„        IIS   1B|I6  18  20  21   25  17   28  29   80    1 

S     8     9    11  IS  [IS  11    22  24  28  27    1     4     5     6     1 

S 

,9    10 

11    12 

1*. 

1  '  1  __■! 

:  :::::  :_:  i  ~:    :   _l 

: 

|       1 

1 

*  "4fH 

1 

1 

i 

-  H 

^        !     "T 

1 

::::::::::::::::::::::::::::±± 

1       ■ 

140 

4--J-4-          4-4- 

! 

,       ■■ 

130                H 

_    !    ±±X^ 

■ 

i, _.________l.,hll   1 

1   1 

ion    5  _r      *IB 

il                                      ksl 

1 

He 

tassl                                                 BSSSsi 

1 

no             B 

jsssH                  m 

i 

■V 

m  m                 m 

>      I 

loo            m,       «* 

Mm                  m 

' 

Wk 

m    m  -_.-_-    ^kl 

u 

!  Bl           ^r 

iWv    r  ^^aB 

•  Hn             ^ 

M  ■    TrV'-rbsJ    !  ■ 

,t' 

so  :_:::::«:::::tt±:- 

'         illKKlMllllIKU'      .      A*4 

L 

■   wm-         ' ' ' ' '  vj 

to t  :•:  -  ;  - Tjj 

W     •'        l\        1    :     IP'-              ■-'    ™ 

TVS    Z  "•  ' 

W  'M     l  \          m    rs  -  p-t  -  - 

^^ 

T  i     1       (         in  '  !  r  m 

T±    i    T^t  '  iP^h" 

50 

\_->n 

I               ±111       X 

t     ■  !     M  *^"^        i     H     ■  1  ;  !  ; 

40    «"?,';  r~c       -' 

TAUb    60   oo    8     4     8     4     0     0     4     4    15 

„    ,     ,        |  ,     ,          ,     ,     , 
15  15  15    3    3    8     8.1  8    0    0    0     0     4     4.    1     8 

i 

j      8     S 

S  1  S  i8 

ao„J 

1  1-1  W 

Figure  248 

The  shaded  area  represents  the  pulse  deficit;  the  upper  edge  is  the  apex  rate;  the 
lower  edge  is  the  radial  rate.  The  broken  line  indicates  the  range  of  the  "average  systolic 
blood  pressure."  Digitalis  figures  indicate  minims  of  the  tincture  and  drams  of  the 
infusion.  October  13,  admitted  to  hospital.  November  3.  up  in  chair  one-half  hour; 
November  9,  up  in  chair  two  hours.  December  4,  up  in  chair  four  hours;  at  this  time 
she  had  a  crop  of  external  hemorrhoids  which  caused  much  distress. 


304  Treatment 

the  exact  mechanism  underlying  this  form  of  irregularity,  it  is 
pretty  generally  conceded  that  it  indicates  a  normal  myocardium 
that  is  being  overtaxed  or  more  usually  a  very  much  damaged 
heart  muscle  for  which  even  a  moderate  stress  is  too  great.     The 

soundness  of  this  view  is  shown  by  the  facts  that  rest  in  bed  fre- 
quently is  associated  with  at  least  the  temporary  disappearance  of 
the  alternation  and  that  an  alternation  which  is  often  very  much 
in  evidence  when  the  heart  is  beating  at  an  excessive  rate  may 
no  longer  be  capable  of  detection  when  it  is  measurably  slowed. 
Alternation  is  often  a  persistent  matter,  and  it  may  he  impossible 
and  unwise  to  keep  a  patient  in  bed  until  it  disappears.  But 
when  first  discovered  the  patient  should  have  the  benefit  of  an 
absolute  rest  for  at  least  a  few  days.  This  should  he  followed  by 
gradually  increasing  exercise,  the  amount  to  he  determined  by  the 
observations  of  the  physician  as  to  its  effect  on  the  activity  ot  the 
heart. 

It  has  been  pointed  out  that  while  alternation  is  regarded  by 
the  majority  of  observers  as  an  indication  of  defective  contractility, 
it  has  not  been  conclusively  proved  that  this  fundamental  property 
is  alone  at  fault,  ft  is  certain  that  many  cases  are  at  least  asso- 
ciated with  a  defect  of  one  of  the  other  properties,  such  as  con- 
ductivity or  irritability.  It  is  also  known  that  we  can  rarely  produce 
a  change  in  one  of  these  fundamental  properties  without  modifying 
the  others.  Hence,  it  is  possible  that  by  inducing  a  change  in  the 
irritability  or  the  conductivity  we  may  indirectly  affect  the  properly 
of  contractility. 

The  .above  may  explain  the  divergent  views  in  regard  to  the  use 
of  digitalis  in  alternation.  It  is  advocated  by  some  workers  and 
discountenanced  by  others.  My  own  observations  lead  me  to  be- 
lieve that  it  is  of  distinct  value  in  some  cases  of  alternation,  and 
I  have  never  seen  harm  done  which  I  could  directly  attribute  to 
the  digitalis.  In  a  case  of  alternation  associated  with  auricular 
flutter,  which  I  had  the  opportunity  to  follow  for  many  months, 
digitalis  was  of  undoubted  value.  In  those  cases  in  which  digitalis 
slows  the  ventricular  rate,  it  will  often  abolish  an  alternation.  Digi- 
talis is  usually  contraindicated  in  the  psuedo-alternans  due  to  extra- 
systoles. 

My  custom  is  to  use  digitalis  in  moderate  doses,  watching  the 


TkhA'l  MEN! 


305 


effect  closely  and  stopping  if  after  a  rea  onable  period,  if  the  heart 
docs  noi  respond  favorably. 

hi  view  of  the  lad  thai  alternation  is  experimentally  readily 
produced  by  certain  poisons,  it  serins  logical  thai  we  should 
reel  as  far  as  possible  disorders  of  metabolism  or  other  sources 
of  toxins,  or  at  least  secure  their  elimination  as  rapidly  as  may 
be.  The  correction  of  kidney  and  bowel  functions  not  only  assist 
in  removing  poisons,  but  also  tend  to  diminish  the  work  winch 
the  heart  is  called   upon   to   perform. 

According  to  Lewis,  patients  witb  alternation  are  not  favorable 
subjects  for  general  anaesthesia.  If  an  anaesthesia  must  be  used, 
ether,  rather  than  chloroform,  should  be  employed. 


BIBLIOGRAPHY 
BOOKS  AND  MONOGRAPHS 

Cusiiny:   Pharmacology.    Third  edition.     Philadelphia.     1903. 

Cyon:    Les  Nerfs  du  Caeur.     Paris.     1905. 

Cyriax:   Kellgreris  Manual  of  Treatment.    London.     [903. 

Gravier:    L'Altemance  du  Caeur.     Paris.     [914. 

Hirschfelder :    Diseases  of  the  Heart  and  Aorta.     Second  edition. 

Philadelphia.    191 3. 
Hoffmann:  Die  Electrocardiographic.    Wiesbaden.     1^14. 
Hofmann:     Remedial   Gymnastics   for   Heart   Affections.      New 

York.      1  y  1  1. 
I  vgic:    (  Editor)  Handbuch  dcr  Pathologie,  Diagnostik  and  Thera- 

pie  Herz  and  Gefdsserkrankungen.    Leipzig.     1914. 
Kaiin:    Das  Electrocardiogram.     Wiesbaden.     i«M4- 
Kraus  i'.m)  NTicolai:    Das  Electrocardiogram  des  gesunden   und 

kranken  Menschen.    Leipzig.     1910. 
Krehl:    Die  Erkrankungen   des  Herzmuskels  mid  die   nervosen 

Herzkrankheiten.     Second  edition.     Wien.     1913. 
Le  Clerq:    Maladies  du  cceur  et  de  I'aorta.     Paris.     1914. 
Lewis:    Mechanism  of  the  Heart  Beat.     London.     191 1. 

Lectures  on  the  Heart.     New  York.     191 5. 
Mackenzie:    The  Study  of  the  Pulse.     London.     1902. 

Diseases  of  the  Heart.     Third  edition.     London.      1914. 
Meyer:   Die  Digitalis  Therapie.    Jena.     1912. 
Meyer  und  Gottlieb:   Die  experimentelle  Pharmakologie.     Wien. 

19 1 4. 
Nicolai  :    Die  Mechanik  des  Kreislaufs.     Nagel's  Handbuch   der 

Physiologie  des  Menschen.    Braunschweig.     1909. 
Ritchie:    Auricular  Flutter.     New  York.     1914. 
Tawara:   Das  reizleitende  System  des  Sdugethier-Herzens.    Jena. 

1 906. 
Tigerstedt:    Human  Physiology.     Third  edition.     Translated  by 

Murlin.     New  York.     1906. 
Wenckebach  :    Die  Arrhythmia  als  Ausdruck  bestimmter  Func- 

tionsstorungen  des  Herzens.     Leipzig.     1903. 
W'iggeks:    Circulation  in  Health  and  Disease.     Philadelphia.     1  y  1 5 . 

306 


Bibliographv 

HEART    BLOCK 

Rachmann:  Jour.  Exp.  Med.,  1912,  xvi,  25. 

BARRINGER:    Arch.  Int.  Med.,   [909,  iv,   186. 

Cohn:    Heart,  1912-13,  iv,  7;  1914,  v,  5. 

Christian:   Arch.  Int.  Med.,  1915,  xvi,  341. 

Edes:    Trans.  Assn.  Amcr.  Phys.,   igoi,  xvi,  521. 

Eppinger  und  Rothberger:  Ztschr.  f.  klin.  Med.,  [910,  lxx,  1. 

Erlanger:   Johns  Hopkins  Hosp.  Bull.,  1905,  xvi,  234. 

Jour.  Exp.  Med.,  1905,  vii,  676;  1906,  viii,  58. 

Amer.  Jour.  Physiol.,  1905-6,  xv,  153. 

Amcr.  Jour.  Med.  Sc,  1908,  exxxv,  797. 
Eyster  and  Meek:   Heart,  1914,  v,  1 19. 
Faiir  :    Virch.  Arch.  f.  path.  Anat.,  1907,  clxxxviii,  562. 
Geriiardt:    Dent.  Arch.  f.  klin.  Med.,  1908,  xcii,  485. 
Hart:   Amer.  Jour.  Med.  Sc,  1915,  cxlix,  62. 
Herrick  :   Amcr.  Jour.  Med.  Sc,  1910,  exxxix,  246. 
Hewlett:    Jour.  Amcr.  Med.  Assn.,  1907,  xlviii,  47. 
James:   Amcr.  Jour.  Med.  Sc,  1908,  exxxvi,  469. 
Krumehaar:    Arch.  Int.  Med.,   1910,  v,  583;   1914,  xiii,  390. 

Univ.  Penn.  Med.  Bull.,  1908. 
Lea:  Lancet,  1915,  i,  1289. 

Lewis  and  Oppenheimer:    Quart.  Jour.  Med.,  191 1,  iv,  145. 
Neuhof:   Amcr.  Jour.  Med.  Sc,  1913,  cxlv,  513. 

Jour.  Amcr.  Med.  Assn.,   1914,  lxiii,  577. 
A.  Oppenheimer  and  R.  S.  Oppenheimer:    Proc  X.   Y.  Patli. 

Soc,  1913,  xiii,  123. 
Oppenheimer  and  Williams:    Proc.  Soc  Exp.  Biol,  and  Med.. 

1913,  x,  86. 
Pardee:    Arch.  Int.  Med.,  1913,  xi,  641. 
Price  and  Mackenzie:    Heart,  1911-12,  iii,  233. 
Thayer:   Arch.  Int.  Med.,  1916,  xvii,  13. 
Wilson:    Jour.  Amer.  Med.  Assn.,   191 5,  lxv,  955. 

extrasystoles 
Danielopolu:   Arch.  d.  mal.  du  cceur,  1914,  vii,  174. 
Dresbach  and  Munford:    Heart,  1913-14,  v,  197. 
Erlanger:    Amcr.  Jour.  Physiol.,  1906,  xvi,  160. 
Ferralis  and  Pezzi  :   Arch.  d.  mal.  du  ca-ur,  1916.  ix,  1. 


308  BlBLldiJRAPHV 

Flemming:    Quart.  Jour.  Med.,  [911-12,  v,  318. 
Gallavardin  and  Gravier:    Lyon  Med.,  [914,  cxxii,  830. 

LaSLETT:     Heart.    l'Mi-lo,    i.    83. 

Levi  :    Heart.  [913-14,  v,  299. 
Lewis  :   Heart,  [910,  ii,  27. 

Quart.  Jour.  Med..  [9]  i-u.  v,  1. 

Heart,  1913-14,  v,  335. 
Lewis  and  Silberberg:    Quart.  Jour.  Med..  1912,  v.  333. 
Lewis  and  White:   Heart.  [913-14,  v,  335. 
Mackenzie:    Quart.  Jour.  Med..  [907-8,  i,  [31  ;  481. 
Rothberger   and  Winterberg:    Arch.  f.  d.  gcs.  Physiol.,    [912, 
cxlvi,  385  :  [913,  cliv,  ^j  1. 

Zentralbl.  f.  Physiol.,    [906,  xxiv,   1. 

VlNNIS:    Heart.   [912-13,  iv,   123. 

Wilson:   Arch.  Int.  Med.,  [915,  xvi,  989. 

TACHYCARDIA 

Cohn:   Jour.  Exp.  Med.,  [912,  xv,  49. 

COHN   AND   FrASER:    Heart.    H)i;v  V,  93. 

Gallavardin:  Arch.  d.  mal.  du  ea-ur,  1916,  ix,  45. 

I  I  \kt  :    Heart.   [912-13,  iv,   128. 
1  [UME  :     Heart.   [9]  [-12,  iii.  89. 

Lea:    Proc.  Royal  Soc.  Med.  (Lond.),  1913.  vi,   U- 
Lewis  and  Schleiter:   Heart.  [911-12,  iii,  173. 
Lewis  and  Silberberg:    Quart.  Jour.  Med..  [911-12,  v,  5. 
LlAN:   Arch.  d.  Dial,  du  ea-ur,  1915,  viii,  193. 
Parkinson  and  Mathias:    Heart,   [914-15,  vi,  27. 
Riiil:    Dcut.  med.  Wchnschr.,  1907,  xxxiii,  632. 
Robinson:   Areli.  Int.  Med.,  [915,  xvi,  967. 
Rothberger  and  Winterberg:  Zentralbl.  f.  Physiol.,  1907,  xxv,  1. 
Arch.  j.  d.  i/es.  Physiol.,   [911,  cxlii,  461. 

auricular  flutter 

Fulton:    Arch.  Int.  Med.,  1913,  xii,  475. 

Hay:    Lancet,  1913,  ii,  986. 

Hertz  and  Goodhart:    Quart.  Jour.  Med..   [908-9,  ii,  213. 

Hewlett  and  Wilson:   Arch.  Int.  Med..  [915,  xv.  786. 

Hirschfelder :    Bull.  Johns  Hopkins  Hosp.,   [908,  xix.  322. 


I  llBLIOGRAP]  I  ,  309 

Hume:    Quart.  Jour.  Med.,  [913,  vi,  235. 

Heart,   [913  14,  v,  25. 

Jolly  and  Ritchie:   Heart,  [910-11,  ii,  177. 

LEVINE  AND   FrOTHINGHAM  :    Arch.  Int.   Med..    I'jI.S.  xvi,  818. 

Lewis  :   Heart ,  igi  2,  iv,  171 . 
M.  c  Willi  am  s  :   Jour.  Physiol.,  [887,  viii,  296. 
Mathewson  :    Edinb.   Med.  Jour.,    [913,  xi,  500. 
Morison  :   Lancet,  [909,  i,  39;  77. 
Neui-iof:   7I/V(/.  Record,  [915,  lxxxviii,  995. 
Parkinson  and  Mathias:    Heart,  [915,  vi,  27. 
Rii-i'l:   Ztschr.  f.  exp.  Path.  u.  Therap.,  [9]  i,  ix,  277. 
Ritchie:    Edinb.  Med.  Jour.,  ](>\2,  ix,  485. 
/'roc.  Royal  Soc.  Edinb.,   1905,  xxv,   1085. 
Robinson:    7oMr.  y^.r/'.  Med.,  u)\t,,  xviii,  704. 
White:  ^;t/;.  /;//.  Med.,  191 5,  xvi,  517. 

auricular  fibrillation 
Agassiz:    Heart,  1912,  iii,  353. 
Busquet:  Presse  uied.,  1914,  xxii,  41. 
Cohn:    Heart,  1913,  iv,  221. 
Cohn  and  Lewis:   Heart,  1913,  iv,  15. 
Cowan:    Glasgow  Med.  Jour.,  1914,  lxxxi,  128. 
Cushny  and  Edmunds  :    Anicr.  Jour.  Med.  Se.,  1907,  exxxiii,  66. 
Draper:    Heart,  1911-12,  iii,  13. 
Eiirenreich  :   N.  Y.  Med.  Jour.,  1914,  xcix,  269. 
Einthoven  and  Korteweg  :    Heart,  1915,  vi,  107. 
Falconer  and  Dean  :    Heart,  1912,  iv,  87. 
Fredericq:    Scalpel,   1914-15,  lxvii,  49. 
Garrey  :   Amer.  Jour.  Physiol.,  1914,  xxxiii,  397. 
Hart:   Med.  Record,  1911,  lxxx,  2. 

Hart  and  James:    Amer.  Jour.  Med.  Sc,  1914.  cxlvii,  63. 
Hering:    Munch,   med.   Wchnschr.,    1912,   lix,   750;  818. 
Hewlett:    Heart,   1910,  ii,   107. 

Arch.  Int.  Med.,  1915,  xv.  786. 
Kilgore:  Arch.  Int.  Med.,  1915,  xvi,  939. 
Lea:    Quart.  Jour.  Med.,  1911-12,  v,  388. 
Lewis:    Heart,  1909-10,  i,  306;  1912-13.  iv,  273. 

Jour.  Exp.  Med..   10 12,  xvi,  395. 


jio  Bibliography 

Lewis  and  M a<  k  :    Quart.  Jour.  Med.,  [910,  iii.  273. 
Lewis  and  Schleiter:    Heart.  [912,  iii,  173. 
Mackenzie:   Brit.  Med.  Jour.,  1911,  ii.  869;  969. 

Quart.  Jour.  Med..   [907-8,  i,  38. 

Atner.  Jour.  Med.  -V(-.,    I«K>7.  exxxiv,    [2. 

Morat  and  Petzetakis:   Compt.  rend.  Soc.  </<•  /•/<</.,  1 « >i 4,  lxxvii. 

■  .  .  ■    .  ■>  - 
—  .  _vV . 

Pardee:   /cur.  Atner.  Med.  Assn.,  1915,  Ixiv,  -057. 

.!/('</.  Record,   1915,  lxxxvii,  710. 

Run.:   Ztschr.  f.  exp.  Path.  u.  Therapy  [910,  viii,  446. 

Robinson:   /o«r.  /-.'.r/\  Med.,  1913,  xviii,  704. 

./>■<■//.  />//.   Med.,    1914,  xiii,  298. 
Rothberger   ami   Winterberg:    Arch.  f.  d.  ges.   Physiol.,   1910, 
exxxi.  387. 

Wien.  klin.  Wchnschr.,  1909,  xxii,  839. 
Wenckebach  :  Arch.  f.  Anat.  11.  Physiol.,  1007,  1-24. 
Wiggers:    Arch.  Int.  Med.,  1915,  xv,  jj. 
Winterberg:    Arch.  f.  d.  ges.  Physiol.,   1901;,  exxviii,  471. 

VENTRICULAR    FIBRILLATION 
GUNN  :    Heart,    KJ13-14,  v,    I. 
Halsey  :    Heart,   11)15,  v'-  67. 
Hoffmann:   Heart,  1912,  iii,  213. 
Levy:   Heart.  1912-13,  iv,  319;  1913-14,  v,  299. 

/owr.  Physiol.,  191 4,  xlix,  54. 
Levy  and  Lewis:    Heart,  1912,  iii,  99. 
McWilliam:    Brit.  Med.  Jour.,   1889,  i,  6. 
Morat  ami  I'i.tzetakis:    Compt.  rend.  Soc.  de  Biol.,  1914,  lxxvii, 

222  ;  237. 
Nobel  ami  Rothberger:  Ztschr.  f.  </.  ges.  exp.  Med.,  1914,  iii,  151. 
Robinson:   /owr.  /;.r/\  .!/.'</.,  1012,  xvi,  291. 

SINO-AURICULAR    BLOCK 

Erlanger:  Amer.  Jour.  Med.  Sc,  1908,  exxxv,  797. 
Eyster  and  Evans:  Arch.  Int.  Med.,  1915,  xvi,  832. 
Gibson:    Practitioner,  1907,  lxxviii,  589. 

Hewlett:    Jour.  .Inter.  Med.  Assn.,  1007,  xlviii,  47. 
Joa<  11 1  m  :    Pent.  Arch.  f.  klin.  Med..  [905,  lxxxv,  373. 
Laslett:    Quart.  Jour.  Med.,  1908-9,  ii,  347. 


Bibliography  31 1 

Levine:  Arch.  Int.  Med.,  [916,  xvii,  15.3. 

Mackenzie:  Brit.  Med.  Jour.,  [902,  ii,  [911. 

Km  1.:    Drill.  Arch.  f.  klin.  Med.,    [908,  xciv,  286. 

Schott:   Munch,  med.  Wchnschr.,  1912,  lix,  -";-'. 

Wenckebach:   ^(rc/i.  /.  .///<//.  u.  Physiol,  [906,  297-354. 

HEART  BLOCK   AND  AURICULAR   FIBRILLATION 

C'oiin:    Heart,   1911-12,  iii,  23. 

Cohn  and  Lewis:  Heart,  1912-13,  iv,  15. 

Draper:    //mr^,  1911-12,  iii,  13. 

Erlanger  and  I  [irschfelder :   Amcr.  Jour.  Physiol.,   1905-6,  xv, 

'  53- 
Falconer  and  Dean:   Heart,  1912-13,  iv,  87. 

Hart:   Amcr.  Jour.  Med.  Sc.,  1 9 1 5 ,  cxlix,  62. 

1 1  ume:   Heart,  1914,  v,  149. 

Lea:    Quart.  Jour.  Med.,  1912,  v,  388. 

Lewis:  Heart,  1909-10,  i,  351;  1911-12,  iv,  15. 

Lewis  and  Mack:    Quart.  Jour.  Med.,  1909-10,  iii,  273. 

Mackenzie:    Heart,  1909-10,  i,  23. 

Price  and  Mackenzie:    Heart,   1912,   iii,  233. 

Souques  and  Routier:   Arch.  d.  mal.  dit  cceur,  1913,  vi,  305. 

White:    Bost.  Med.  and  Surg.  Jour.,  1915,  clxxiii,  431. 

nerve  control  of  the  heart 
Aschner:    Wien.  klin.  Wchnschr.,  1908,  xliv,  1529. 
Cohn  :   Jour.  Exp.  Med.,  1912,  xvi,  732;  1913,  xviii,  715. 
Cohn  and  Fraser:    Heart,  1914,  v,  93. 
Dogiel:    Arch.  f.  d.  gcs.  Physiol.,   191 I,  cxlii,    109. 
Erlanger  and  Hirschfelder:    Amcr.  Jour.  Physiol.,  1905-6,  xv, 

153- 
Fabre  and  Petzetakis  :    Compt.  rend.  Soc.  de  Biol.,  1914,  lxxvi, 

343- 
Ferralis  and  Pezzi  :   Arch.  d.  mal.  du  cceur,  1916,  ix.  1. 
Ganter  and  Zahn  :  Arch.  f.  d.  ges.  Physiol.,  1913,  cliv,  492. 
Hart:    Amcr.  Jour.  Med.  Sc,  1915,  cxlix,  66. 
Keith  and  Flack:   Jour.  Anat.  and  Physiol.,  1907.  xli,  172. 
Levine:   Arch.  Int.  Med.,  1915.  xv,  758. 

Loeper  and  Mougeot:   Compt.  rend.  Soc.  de  Biol.,  1914,  lxxvi,  104. 
Meek  and  Eyster:   Heart,  1914,  v,  22-j. 


312  Bibliography 

Mines:  Jour.  Physiol.,  mi  \.  xlvii,  4m. 
Muskens:    Amer.  Jour.  Physiol.,   [898,  i.  486. 

1  IPPENHEIMER  AND  (  IPPENH  I.I  M  ER  :    Jour.  Exp.  Med.,   1  < )  I  _\  XVi,  613. 

I'i.  iv.  1  1  akis  :  Bull.  et.  mem.  soc.  med.  d.  hop.  de  Paris,  1914,  xxxvii, 

73!  '■ 
Rit<  hie:    Quart.  Jour.  Med.,  1912-13,  vi,  <>_>. 

Robinson:   Arch.  Int.  Med.,  [915,  xvi,  967. 

Robinson  and  Draper:    Jour.  Exp.  Med.,  1911,  xiv,  217;   1912, 

xv,  14. 

ROTHBERGER    AND    WlNTERBERG :     Arch.    f.    d.    ges.    Physiol.,     I9IO, 

cxxxv,  506;  559;    I'll  1.  cxli,  217;  343. 
Wilson:   Arch.  Int.  Med.,  1915,  xvi,  1008. 

ALTERNATION 

Esmein  :  Arch.  d.  mal.  du  cceur,  1913,  vi,  385. 
Gallavardin  am>  Gravier:   Arch.  d.  mal.  du  carur,  1914,  vii,  497. 
Lvo«  Mi  (/..  i«)ii.  1  )ec.  [9. 

(i  M.1.1  :    Arch.   d.   mal.  du   Civur,    [916,   ix,  40. 

Hering:    Ztschr.  f.  exp.  Path.  u.  Therap.,  1912,  x,  14. 

Herrick:  Jour.  Amer.  Med.  Assn.,  1915,  Ixiv,  739. 

Joachim:    Munch,  med.  Wchnschr.,   1911,  lviii,   1951. 

Kahn:    Arch.  f.  d.  ges.  Physiol.,    [911,  cxl,  471. 

Lewis:   Quart.  Jour.  Med.,  1910-1  1,  iv.  141. 

Muskens:   Jour.  Physiol.,  1907,  xxxvi,  104. 

Pezzi  and  Douzelat:   Arch.  d.  mal.  du  cceur,  i<M4.  vii.  81. 

Km  1.:    Ztschr.  /'.  exp.  Path.  u.   Therap.,   1906,  iii.  275. 

Vaquez:    XVII,  Internat.  Congr.  Med.,  London,   [913,  vi,  157. 

White:    Amer.  Jour.  Med.  Sc,    1915,  cl,  82. 

Windle:    Quart.  Jour.  Med.,   mho,  iv,  435;   [912,  vi,  453. 

DIGITALIS 
Bailey:   Jour.  Pharmacol,  and  Exp.  Therap.,  1909,  i.  349. 
Ciikistiax:    Arch.  hit.  Med.,  1915,  xvi.  341. 
Cohn:    /owr.  Amer.  Med.  Assn..    \^^.  Ixv,    1 5-7- 
Cohn,  Fraser  and  Jamieson:    /owr.  Exp.  Med..   [915.  xxi-  593- 
Cushny:   /our.  /:.r/\  .l/r</.,  [897,  ii.  233. 
Cushny,  Marris  and  Silberberg :    Heart,  KJI2.  iv,  I. 
Danielopolu:   Compt.  rend.  soc.  dc  biol.,  1913,  Ixxiv,  969. 
Eggleston:   Arch.  hit.  Med..  i<M5,  xvi,  1. 


Bibliography  313 

Gottlieb  :  Med.  Klinik,  [913,  ix,  2061. 

Hart:    L.  I.  Med.  Jour.,  [913,  vii,  217. 

Hatcher  and  Bailey:  Jour,  Amer.  Med.  Assn.,  [907,  xlviii,  1177. 

Hatches  and   Eggleston:    Jour.  Pharmacol,  and  Exp.  Therap., 

\<)\J,   iv,  97. 

Hewlett  and  Barringer:   Arch.  Int.  Med..  [910,  v,  93. 
James  and  Hart:   Amer.  Jour.  Med.  Sc,  [914,  cxlvii,  63. 
Janeway:    Amer.   Jour.    Med.   Sc,    L908,   exxxv,    781. 
Lehnert  anii  Loeb  :    Therap.  Monatsh.,  1914.  xxviii,  164. 
Mackenzie:    Heart,   [911,  ii,  273. 
Martinet:    Presse  med.,   i<)i4,  xxiii,  361;  433. 
Reinike:    Ztschr.  f.  klin.  Med..  [913-14,  lxxix,  441. 
Roth:   Bull.  Hyg.  Lab.,  U.  S.  P.  H.  and  M.  II.  S.,  Xo.  102. 
Rotiiberger  and  Wi  NTERBERG :    Areh.  f.  d.  (jcs.  Physiol.,  1913,  cl, 

217. 

Schleiter:    Amer.  Jour.  Med.  Sc.,  T914,  cxlviii,  343. 
Voegtlin    and    Macht:     Jour.    Pharmacol,    and    Exp.    Therap., 
I9I3-M,  v,  76. 


INDKX 


a   wave,    15,    [6. 

(l-c  interval,  44. 

variations  in,  210. 

and  digitalis,  205. 
Accelerated  heart,  82,  245. 

clinical    significance,  88. 

contractility   in,  86. 

electrocardiograms,  89. 

etiology,  82. 

identification,  86. 

mechanism,  85. 

pathology,  83. 

polygrams,  87. 

prognosis,  88. 

toxins,  83,  84. 

treatment,  284. 
Accelerator  nerves,  6,  30,  200. 

in  auricular  fibrillation,   136. 

in  auricular  Mutter,  118,   122. 

in  rapid  heart,  83,  84. 
Aconite,  34,  92,  180. 
Action  current  of  heart,  19. 

direction  of,  236. 
Adams-Stokes   syndrome,  40,   42,   52, 
54.  229. 

and  heart  block,  53,  55,  230. 
Adrenalin,  34,  61,   172,  260,  283. 
Alcohol,  95,  140,  184,  261,  285,  293. 

in  heart  block,  51. 
Alternation,  27,  180. 

age  incidence,   184. 

and  flutter,   184. 

and  tachycardia,   189. 

clinical   features,   194. 

conductivity  in,  181. 

contractility  in,  181. 

duration,   194. 

electrocardiograms,  183,  192,  197. 

etiology.   182. 

excitability  in.   181. 

experimental  production,  180. 

identification,   186. 

mechanism,   181. 

pathology,  181. 

polygrams  of,   183,  185,  189. 

post-extrasystolic,  186,  194. 

prognosis,  196. 

treatment,  302. 
Ammonia,  261. 
Anatomy,  3. 
Angina  Pectoris,  249. 
Antiarin,  180. 
Aortic  bulb,  13. 
Aortic  Stenosis,  31. 
Apocynum,  264. 
Arrhythmias :    mixed,  222. 

block  and  extrasystoles,  230. 

fibrillation  and  block,   226. 

fibrillation  and  extrasystoles,   224. 

sinus  and  conduction  defects,  222. 
Arterial  Pressure,  30,  ^2>  9~- 


(See  also  "hypertension" ) 

in  auricular  fibrillation,  167,  303. 
Arterio-sclerosis,  114.  228,  2  0 

and  alternation,   186. 

and  fibrillation,   139,  140,   [68 
Asphyxia,  34. 
Asthma,  250. 
Atheroma,  35. 

Atropine,   32,  61,   214,  220,  262. 
and  digitalis,  280. 
heart   block  in,  50,  229. 
hypervagotonics  in,  204. 

Auricular  canal,  13. 

Auricular  fibrillation,  38,  102,  116,  [34. 

age   incidence,   138. 

and  arterio-sclerosis,   139,   140,    [68. 

and  block,  226. 

and  extrasystoles,  141,  160,  170,  171. 
224. 

and  flutter,  173. 

and  rheumatism,   139,   160,   168. 

and  sinus  arrhythmia,  218. 

and  tachycardia,   173. 

and  vagus,   137. 

and  valvular  disease,  138,  140. 

arterial  tracings,  143. 

clinical   features  of,   156. 

digitalis  in,   136,   137,  268,  270.   272, 
293,  300. 

due  to  toxins,   138. 

electrocardiograms,    148,    151,    153, 
155- 

etiology,  138. 

experimental  production,   135. 

heart   rate   in,   160. 

His'  bundle  in,  152. 

identification.    141. 

mechanism,   136. 

murmurs  in,   142,   144. 

paroxysmal,   158. 

pathology,  138. 

polygrams,  145,  146. 

prognosis  in,  170. 

pulse  deficit  in,  162. 

treatment.   170,  292,  300. 
Auricular  flutter,  117,  120,  182. 

age  incidence,   120. 

and  extrasystoles,  118. 

and  fibrillation,   118,    120,   124,   130, 

13^.  173- 
and  heart  block,  124. 
and  tachycardia,   173. 
auricular  rate,   117. 
bundle  of  His  in.  118.  120. 
clinical  course  of,  130. 
conduction   in,   120,   128. 
contractility  in,  120. 
coronary  arteries  in,  122,  124, 
digitalis  in,  272. 
duration,  130. 


315 


l.M'l  X 


trocardiograifis,    123,    125,    126, 
129,  131. 

etiology,  120. 

experimental  production,   1 1  ~- 

identification,  124. 

mechanism,   118,  1 19- 

pathology,  120. 

polygrams,  121,  126,  179. 

significance  of,  132. 

treatment,  288. 

vagus  eff<  d  on,  1 18,  122. 
Auricular  tachycardia,   117.    >7''.   [78. 
Auricular  tachyrhythmia,    1 1  r- 
Auricular  tachysystole,  1 1  r  - 
Auriculo-ventricular  bundle,  4.  5.  14 
26,  -•:. 

i  Si  <■  also  I  lis'  bundle  > 

branches,  5. 
Auriculo-ventricular   node,   4.   5i   -'■ 

30. 
.1-1'  bundle, 

(  Sir  "I  li-*  bundle"  I 

in  auricular  fibrillation,  168. 

defects  in,  222. 

digitalis  effect  on,  268. 
Bathmotropic  influences,  10. 
Baths,  258. 
Beer  heart,  256. 
Beverages,  257. 
Blood-letting,  253. 

Blood  pressure,  166. 

average  systolic,  167,  171.  300. 

digitalis  effect  on.  300,  303. 

in  alternation,   is<>.   194. 

in  auricular  fibrillation,  165,  170. 
litch's  Law,  II,  12,  102. 
Bradycardia.   27,  31. 

nodal.  226. 
Bromides.  284,  287. 
r  wave,  15,  16. 
Caffeine,  263. 

( Calcareous  degeneration,  35. 
(  amphor,  263. 
( lardiogram 

inverted,  18. 

bral  hemorrhage,  31,  88. 

turners.  31. 
Cheyne-Stokes  respiration,  132. 
Chloroform,  172,  204,  284,  305. 

in  heart  Mock.  51. 
Chronotropic  influences,  9. 
Classification    of    myocardial    disturb- 
ance - 
Coffee,  283,  285,  293. 
( '■  1*1  applications,  258. 
Compensatory  pause,  58,  66. 

complete,  58. 

incomplete,  58.  66. 
Complete    irregularity,    27,    lor>,    141, 
154- 


(See  aUo  "auricular  fibrillation") 

of  sinus  origen,  216,  219. 
Conduction,  27,  33. 

1  S(  <■  "stimulus  conduction"  1 

after  digitalis,  266. 

delayed,  34,  47. 

impaired,  36,  120.  12S,   181,  2-2. 

increased,  85. 

rati-  of,  20. 
Conductii  n   system,  5.  35. 

path  of,  29. 
Contractility,  8,  9,  1 1.  24.  26. 

abolished,   13. 

diminished,  86,  181. 

in    auricular    flutter,    120. 

Convallaria,  204. 

Coronary  arteries,  92,  94  ti2. 

in   auricular   fibrillation,    138. 

in   auricular   flutter,    122.    124. 

in  ventricular   fibrillation,    171. 
Coupled   rhythm,  64,  268,  296. 
Cribbing,  210.  213. 
Dclerium  cordis,  134. 
Dextrocardia,  237. 
Diet.  254. 

Karell,  2^7. 
Digitalis,  27.  .,4.  36,  38,  ',<>.  264. 

and  atropine,  280. 

and  blood  pressure,  300,  303. 

and  sinus  arrhythmia,  220. 

bigeminus,  64. 

coupled  rhythm.  64. 

dosage,  273. 

effect  on   T  wave.  270,  300. 

in  alternation.    180,   304 

in  auricular  fibrillation,     13  >.     170, 
224.  293,  294,  300. 

in  auricular  flutter,    130.    133,   290. 

in  extrasy stole,  60,  61.  283,  284. 

in  heart   block,   50.  228. 

in  tachycardia,  286. 

trigeminus,  64. 
Dilatation.  1,  12,  85,  170. 

acute.   2  |o. 

Diphtheria,  36,  54.  12-'.  184, 
Dissociation,  32. 

complete,  33. 

incomplete,  34. 
Dromotropic  influences,  n. 
Dropped  beat,  34.  42,  40.  56,  215. 

/;    interval.    1 7. 

Einthoven's  ( ralvanometer,  10. 

electrodes,  20. 

standardization,  20.  21. 
Electrocardiogram,  15. 

after  atropine.    279,  281. 

after  digitalis,    207.    269,    271,   291, 

299. 
compared  with  polygram,  24,  25. 
comparison    in   different    leads,    24. 

234- 


I ;, i >{■.:■: 


V7 


method  of  taking,  10. 

normal,  23,  24. 

of  accelerated  heart,  89. 

"i"  alternation,  [83,   tp3,   [95,  107- 

of  auricular  fibrillation,  tip,  i.;i . 
[51,  153,  155)  l57)  ''".  [°3<  169, 
174,  175,  240. 

of  auricular  flutter,  [23,  125,  127, 
1 21 1,   [31,  29 1 . 

nf  block  and  extrasystoles,  231, 

of  delayed  conduction,  47,  223,  267. 

of  dextn  cardia,  237. 

of  extrasystole,  68,  71,  72,  73,  75, 
77,  70,  81,  [29,  159,  [61. 

of  fibrillation  and  Mock,    225,    227. 

of  fibrillation  and  extrasystoles, 
225,  299,  301. 

of  flutter   and   tachycardia,    177. 

of  heart  block,  44,  45,  48,  49,  279. 

of  hypertrophy,  239,  241. 

of  infants,  240. 

of  lesion  of  limb  of  His'  bundle, 
233. 

of  paroxysmal  tachycardia,  105, 
107,   109,  in,   113,   115. 

of  sinus  arrhythmia,  209,  211,  215, 
223. 

of  vagus  pressure,  203,  289. 

standardization,  20. 
Electrocardiograph,   2,    19. 
Electrodes,  20. 
Embryonic  heart,  3. 
Epinephrin,  206. 
Erlanger  apparatus,  18. 
Escape  of  the  ventricle,  34,  206. 

in  heart  block,  46. 
Esophageal  records,   19. 
Excitability,  8,  9,  10,  11,  14,  26,  32. 

abolished,  13. 

increased,  61,  85,  90. 
Exercise,  83,  248,  304. 

and  extrasystoles,  62. 
Extracardial   nerves,    30,    32,    83,    85, 
199. 

(See  also  "vagus"  and  "accelera- 
tors") 

anatomy,   199. 

distribution,  201. 

physiology,  200. 
Extrasystole,  27,  38,  56. 

after  digitalis,  268. 

allodrome,  60. 

and  block,  230. 

auricular,  58,  65,  66,  70,  73,  176. 

bigeminus,  63. 

clinical  significance,  78. 

electrocardiograms,  68,  71,  72,  73. 
/5.  77,  79- 

etiology,  57. 

experimental  production,  60. 


identification,  62,  218. 

in  Mm  ill.ii  ion,  224. 

interpolated,  78,  79. 

mi  1  hani  tm,    9, 

nodal,  66,  67,  76,  77,  78. 

noi  modrome,  60. 

pathology,  $7. 

polygrams,  65. 

prognosis,  80. 

treatment,  2X2. 

trigeminus,  64. 

types,  74,  75,  81. 

ventricular,   58,  67,  68,  69,   72.  73, 
74,  71,  77,  296. 
Fear,  248. 
Fevers,  31,  36.  53,  84,  249. 

and  alternation,  184. 

and  fibrillation,   140. 
ff  oscillations,  152,  154. 
Fibrosis,  35,  94. 
Frog's  heart,  3,  13. 
Galvanometer,  19. 

electrodes,  20. 

standardization,  20,  21. 
Glyoxilic  acid,   180,   182. 
Graphic  records,  15,  27, 

esophageal.  19. 
Graves'  disease,  84,  87,  96,  272. 

and  sinus  arrhythmia,  215. 

fibrillation  in,  140. 
h  wave,  15,  16. 
Haemolytic  serum,  180. 
Heart 

action  current  of.  19. 

change  in  position,  234. 

cycle.  245. 

disposition  of  muscle,  234. 

frogs,  3,   13. 

hypertrophy,  236,  245,  249. 

insufficient.   244. 

irregular,   27. 

normal,  28. 

outside   demands  on.  82. 

rate  of.  14,  27.  28,  38. 

regular,  27. 

reserve  force,  244.  246. 

rhythm.  27,  28. 

small,  250. 

valves  of,  1. 
Heart  block,  31,  32. 

(see  also  dissociation.) 

a-c   interval,   44. 

Adams-Stokes    syndrome,    40.    42, 
230. 

and  extrasystoles,  230. 

and  fibrillation.  226. 

and  sinus  arrhythmia.  46.  220. 

atropine  in,  278. 

auriculo-ventricular.   14. 

clinical  features,  50. 


:i8 


t~NDEX 


complete,  3 

course,  53. 

dropped  beats,  46. 

electrocardiogram  in,  44.  47.  4S,  .40. 

etiology,  36. 

following  digitalis,  268,  278. 

identification,  38. 

jugular  vein  in,  40. 

partial,  33,  34,  277. 

pathology,  34. 


»f,  42, 
54- 


43- 


polygram  < 

prognosis, 

rati-.  38. 

significance,  50. 

treatment,  277. 
Hellebore,  264. 

His'  bundle,  4.  5,  14.  26,  27,  33,  34,  200. 
auricular-^  entricular 


t  See      also 

bundle ). 
branches, 

in  auricular 
in  auricular 


232,   233. 

fibrillation,  152,  168. 
flutter,  11N,  120. 

in  heart  block,  50. 
1  [ypersympatheticotonics,  204. 
Hypertension,  .}_'.  92,  -'411.  250,  256. 

digitalis  in,  272. 
Hypertonus,  30,  84. 
Hypertrophy  of  heart,  1,  85,  296. 

left,  236. 

rijjit.  237. 
1 1\  pervag  tonics,  -'04. 
[deo-ventricular  rhythm,  14,  2^2. 
Influenza,  53. 
Inotropic  influences,  11. 
Intermittent  pulse.  56. 
Irregular  heart.  27,  29. 
Irritability,  24. 

after  digitalis,  266,  268. 
Jaundice.  31. 
Jugular  pulse,  15,  40. 

ventricular   form.   134,   142,    140. 
Jugular  vein. 

in  alternation.   190. 

it-   heart   Mock,  40. 

pressure,  -'5. 

records,  15. 
Karell   diet.  257. 
Labile  pulse,  83,  84. 
Law  of  "all  or  ni  tie."  11,  12. 
Leucocytic  infiltration,  35. 
I  i'  bermeister's  rule.  84. 

Mackenzie   cup,    18. 

Maximal  contractions:  law  of.  11,  12. 
Meningitis,  31. 
Mitral  pulse,  134. 
Mitral  stenosis,  138,  139. 

murmurs.    I4_\    144. 
Muscarine,  34.  61.  02. 
Muscle  tremors,   154,   157. 
Myocardium,  1. 


abnormal     function,     classification 

.if,    2''. 

anatomj .  3. 

function.    1. 

fundamental  properties  of,  7, 

in  accelerated  heart.  83. 
infarct-  of,   124.   [84. 

Myogenic  theory,  7. 
Nephritis,  31.   [82,  - 

alternation   in.    [86,    [96. 
diet   in.  256. 
fibrillation  in.  140. 
Nen  1 5. 
see  "accelerators." 
see  "extracardial  nerves." 
see  "sympathetic." 

see'    "vagUS." 

Neurogenic  theory,  <>. 

Nicotine,  61,  05,  285,  2<i:,. 

and  auricular  fibrillation,   136. 

and  extrasystoles,  283. 
Nitrites,  275. 
Nodal  bradycardia,  226. 
Nodal  rhythm,  14.  135. 
Node. 

auriculo-ventricular.  4,  5,   14,  20. 

sino-auricular.  3.  5.   14.  26,  200. 

Tawara's,  4,  5,  14,  26,  200. 
Obesity.  250.  255. 

Oculocardiac  reflex,  204,  205,  220. 
(  Ipium,  274,  287. 
/'  wave.  21,  22.  24,  83. 

ahsence  of,  152. 

changes    in    form,   224. 

reversed,  70,  71,  73. 

/'-A'   interval.  22,  24. 

in  heart  Mock,  44. 

prolonged,  47,  267. 

variable,  22T,,  281. 
Pacemaker  of  heart,  9,  14,  28,  29. 
Pain,  97.  160. 
Palpitation,  78. 

Paroxysmal   tachycardia,  82,  90,   124, 
[58,  194- 

ape  incidence,  95. 

auricular.    104.   108. 

and  auricular  fibrillation,    116,    173. 

and  auricular  flutter,   173. 

and  extrasystoles,  91,  102,   112.   114. 
IIS. 

clinical  significance.  114. 

digitalis  in,  9'',  272. 

duration,  90. 

electrocardiograms,    105,     107,     100. 
in,  113.   115. 

etiology,  95. 
Graves'  disease,  96. 

identification,   100. 

mechanism,  90,  93. 

nodal.   110. 

pathology,  94. 


[ndex 


319 


polygrams,  99,  ioi,  103. 

prognosis,  1  14. 

rate,    ion. 

rhytlnu,   mo. 

symptoms,  96. 

treatment,  285. 

ventricular,  106,  112. 
Pericarditis,  114. 
Pericardium,  1. 
Physiology,  6. 
Physostigmine,  34,  61. 
Pilocarpine,  136,  204. 
Pneumonia,  36,  53,  158,  160,  184. 
Polygram,  15. 

a-c  interval  in  block,  44. 

compared    with    electrocardiogram, 
24,  25. 

delayed  conduction,  41. 

digitalis  effect,  265,  299. 

heart  block,  39,  42,  43. 

method  of  taking,  16. 

normal,  17. 

of  accelerated  hearts,  86. 

of  alternation,   183,   185,   191. 

of  auricular  fibrillation,     145,     147, 
149,  299. 

of  auricular  flutter,  121,  126. 

of  block   and    extrasystoles,   231. 

of  extrasystoles,  65,  67,  69. 

of  fibrillation  and  block.  227. 

of  paroxysmal  tachycardia,  99,  101, 
103,  185. 

of  sinus  arrhythmia,  207,  213,  219. 
Polygraph,  2. 

Post-extrasystolic  pause,  66. 
Pregnancy,  31,  84. 
Premature  beats,   56. 

(see  also  "extrasystole"). 
Pressure  in  chambers   of   heart  and 

vessels,  25. 
Properties  of  Muscle  cells,  7. 

changed,  86. 
Pulse  deficit,  162,  163,  170. 

and  blood  pressure,  165,  302. 

relative.   164. 
Pulsus  alternans,  28,  180. 
Pulsus  arhythmicus.  134. 
Pulsus  bigeminus.  63,  78.  81,  180,  188. 
Pulsus  deficiens,  134,  162. 
Pulsus  frustrans,   31. 
Pulsus  inaequalis,  134. 
Pulsus  intermittens.    134,   162. 
Pulsus  irregularis,   134. 

perpetuus,  156. 
Pulsus  pseudo-alternans.  180,  304. 
Pulsus  trigeminus,  64.  68,  69,  71,  72. 
Purkinje's  fibers.  4,  33. 
Q  wave,  21,  22,  24. 
R  wave,  21,  22,  24. 
Radial. 

in  alternation,  187,  193. 


records,  is. 
Rate  of  heart.  [4,  27,  ! 
Reflexes,  X,  10,  31,  84. 

in  hearl  block,  51. 

oculo-cardiac,  204,  206 
Refractory  period,  1-',  13,  4''.    ' 
Refractory  phase,  58. 
Regular  heart,  27,  29. 
Rest,  244,  304. 

Retrograde  stimuli,  60,  91,  94.  106. 
Rheumatism,  36,  54,  85,  Hj,  95. 

and   alternation,    184. 

and  fibrillation,  139,  160,  228. 

and  flutter,   122. 

extrasystoles  in,  6i,    100. 
Rhythm." 

coupled,  64. 

ideo-ventricular,   14,  33. 

nodal,  14,   135. 
Rhythm  of  heart,  27,  28,  29. 

phasic  variations,  216. 
S  wave,  21,  22,  24,  83. 
Shock,  84. 

Sino-auricular  block,  212. 
Sino-auricular  node.  3,  5.  26. 

(see  also  "sinus-node"). 
Sinus  arrhythmia,  27,  42,  208. 

and  conduction  defects,  222. 

and  heart  block,  46. 

clinical   features,  218. 

electrocardiogram,     209,     217.     221, 
22?. 

identification,  210. 

polygrams,  207. 

respiratory,  206. 

significance,  220. 

treatment,  287. 
Sinus  node,  26,  28.  32,  ~y,  212. 

as  pacemaker,  48. 
Sinus  venosus.  3.  6.  8,  13. 
"Skin  current,"  20,  21. 
Spontaneous  cardiac  contraclions,  14. 
Squills,  264. 

Stannius  experiment,  13.  33. 
Stimulus  conduction,  7,  9.   10.   11.   13, 
24.  26. 

abolished,  13. 

rate,  10. 

retrogade.  60. 
Stimulus   production.  7,  8,  o,    u,  24, 
26.  30. 

heightened,  85. 

variation  in  rate  of,  210. 
Strophanthin.  264. 

in  alternation,  182. 

in  flutter,  290. 

in  tachycardia,  286. 
Strychnine,  275. 

poisoning,  182.  184. 
Sulcus   terminalis,   3. 


[ndex 


Sympathetic  nerves,  86. 

( see  "accelerator  nerves"  I. 

cervical,  [99, 
Syncope,  98. 
Syphilis,  35,  54.  95,  122,  1S4.  292,  298. 

and  fibrillation,  140,  228. 

and  heart  block,  278. 
T  wave,  21,  22.  24.  83. 

after  digitalis,  272,  300,  301. 
T-l'  interval,  _•-',  24. 
Tachycardia,  27 

and  alternation,  [97. 

and  auricular  fibrillation,   173. 

and  auricular  flutter,  [73. 

vagus  pressure,  203. 
Tea,  1N1.  283,  285,  -•').?. 
Teh  cardii  igrams,  21. 
Theobromine,  263. 
Theocin,  263,  283. 
Theophyllin,  263. 
Thyroid  extract,  84,  285. 
Tobacco  heart,  <>_•. 

in  alternation,   [84. 
Tonicity,  8,  n.  12,  _■<>. 
Treatment,  242. 

adrenalin.  26b. 

alcohol,  261. 

ammonia,  261. 

atropine,  _'<>-*. 

baths,  258. 

beverages,  2?j. 

M'"  id  letting,  253. 

caffeine,  263. 

camphor,  263. 

chloroform,  264. 

cold  applications,  258. 

diet,   J54. 

digitalis,  264. 
drugs,  260. 
exercise,  248. 
general  principles.  242. 
heart  block,  277. 
individualization,  243. 

massage,  252. 

modified  by  types  of  rhythm,  276. 

nitrites.  27'-. 

obese,  250. 

of  accelerated   heart,  284. 

of  alternation,  302. 

of  auricular  fibrillation,  202. 

of  auricular  flutter.   288. 

of  extras}  stole,  282. 

of  paroxysmal  tachycardia,  285. 

of  sinus  arrhythmias,  287. 

opium,  274. 

resistance  exercise,  2-2. 

rest,  244. 

spa,  259. 


strychnine,  275. 

sugar  in,  255. 
Tubei  miosis.  84. 

Typhoid  fever.  31,  36,  53,  84,  184 
/ '  wave,  22. 
Uskoff  apparatus,  t8, 

V  wave.    15.    id,    [46. 

Vagus,  6,  30,  32.  34.  36.  38,  92.   [99 
202,  216. 
and  extrasj  stoles,  61. 
atropine  effect  on,  280. 

in   accelerated   heart,  83,  So. 

in   auricular   fibrillation,    [36,    173. 

in  auricular  flutter,   [l8,    122.   173. 

in   heart  block,  50,  51.  280. 

in  sinus  disturbances,  22  \. 

pressure,  202,  214,  220,  286,  _>sx. 
Valerian,  284,  287. 
Valves,  1. 
Valvular  disease,  85,  96,  114. 

and  auricular   fibrillation,   1.58,   139, 
140. 

and  block,  228. 

and  hypertrophy,  241. 
Vaso-motor  disturbances.  84. 
Venesection,  254,  293. 
Ventricular  fibrillation,  171. 

and  extrasystoles,  172. 

due  to  adrenalin.  172. 

due  to  chloroform,  172. 
Veratrin,  182. 
Vertebrate  heart,  3,  13. 
Water  balance,  256. 
Waves. 

cause  in  electrocardiogram,  22. 

size  of,  18. 

time  relations  of.  16,  18,  25. 
Waves  of  electrocardiogram. 

amplitude  of,  236. 

/'.  21,  22.  24. 

".  21,  22,  24. 

A'.  21.   22.  24. 

S,  21.  22,  24. 
/  21  22  24 
U,    22. 

Waves  of  polygram. 
a.  15,  16. 
c,  15.  16. 
/'.  15.  16, 
v,  15.  r6. 

.!'.    I  :,    [6. 
V.    15.    I''. 

Weight,  255. 

(see  also  "obesity"). 

under,  256. 
.v  wave.  15,  to. 

V  wave,  15,  [6. 


Tie  copyright  of  this  hook,  in  oil  English-Speaking 
countries,  is  owned  by  Rebman  Company,  Nctu  )  or/.-. 


H25 
Copy  1 


